Methods used by pathogenic organisms to evade a host's immune system.
Invertebrate organisms that live on or in another organism (the host), and benefit at the expense of the other. Traditionally excluded from definition of parasites are pathogenic BACTERIA; FUNGI; VIRUSES; and PLANTS; though they may live parasitically.
The relationship between an invertebrate and another organism (the host), one of which lives at the expense of the other. Traditionally excluded from definition of parasites are pathogenic BACTERIA; FUNGI; VIRUSES; and PLANTS; though they may live parasitically.
The body's defense mechanism against foreign organisms or substances and deviant native cells. It includes the humoral immune response and the cell-mediated response and consists of a complex of interrelated cellular, molecular, and genetic components.
The interactions between a host and a pathogen, usually resulting in disease.
The capacity of a normal organism to remain unaffected by microorganisms and their toxins. It results from the presence of naturally occurring ANTI-INFECTIVE AGENTS, constitutional factors such as BODY TEMPERATURE and immediate acting immune cells such as NATURAL KILLER CELLS.
Proteins found in any species of protozoan.
The ability of tumors to evade destruction by the IMMUNE SYSTEM. Theories concerning possible mechanisms by which this takes place involve both cellular immunity (IMMUNITY, CELLULAR) and humoral immunity (ANTIBODY FORMATION), and also costimulatory pathways related to CD28 antigens (ANTIGENS, CD28) and CD80 antigens (ANTIGENS, CD80).
A species of protozoa that is the causal agent of falciparum malaria (MALARIA, FALCIPARUM). It is most prevalent in the tropics and subtropics.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Measure of the number of the PARASITES present in a host organism.
The specific failure of a normally responsive individual to make an immune response to a known antigen. It results from previous contact with the antigen by an immunologically immature individual (fetus or neonate) or by an adult exposed to extreme high-dose or low-dose antigen, or by exposure to radiation, antimetabolites, antilymphocytic serum, etc.
Any part or derivative of any protozoan that elicits immunity; malaria (Plasmodium) and trypanosome antigens are presently the most frequently encountered.
Change in the surface ANTIGEN of a microorganism. There are two different types. One is a phenomenon, especially associated with INFLUENZA VIRUSES, where they undergo spontaneous variation both as slow antigenic drift and sudden emergence of new strains (antigenic shift). The second type is when certain PARASITES, especially trypanosomes, PLASMODIUM, and BORRELIA, survive the immune response of the host by changing the surface coat (antigen switching). (From Herbert et al., The Dictionary of Immunology, 4th ed)
The degree of pathogenicity within a group or species of microorganisms or viruses as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. The pathogenic capacity of an organism is determined by its VIRULENCE FACTORS.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
Those components of an organism that determine its capacity to cause disease but are not required for its viability per se. Two classes have been characterized: TOXINS, BIOLOGICAL and surface adhesion molecules that effect the ability of the microorganism to invade and colonize a host. (From Davis et al., Microbiology, 4th ed. p486)
Lymphocytes responsible for cell-mediated immunity. Two types have been identified - cytotoxic (T-LYMPHOCYTES, CYTOTOXIC) and helper T-lymphocytes (T-LYMPHOCYTES, HELPER-INDUCER). They are formed when lymphocytes circulate through the THYMUS GLAND and differentiate to thymocytes. When exposed to an antigen, they divide rapidly and produce large numbers of new T cells sensitized to that antigen.
Non-antibody proteins secreted by inflammatory leukocytes and some non-leukocytic cells, that act as intercellular mediators. They differ from classical hormones in that they are produced by a number of tissue or cell types rather than by specialized glands. They generally act locally in a paracrine or autocrine rather than endocrine manner.
Proteins found in any species of virus.
The continuous sequence of changes undergone by living organisms during the post-embryonic developmental process, such as metamorphosis in insects and amphibians. This includes the developmental stages of apicomplexans such as the malarial parasite, PLASMODIUM FALCIPARUM.
Membrane glycoproteins consisting of an alpha subunit and a BETA 2-MICROGLOBULIN beta subunit. In humans, highly polymorphic genes on CHROMOSOME 6 encode the alpha subunits of class I antigens and play an important role in determining the serological specificity of the surface antigen. Class I antigens are found on most nucleated cells and are generally detected by their reactivity with alloantisera. These antigens are recognized during GRAFT REJECTION and restrict cell-mediated lysis of virus-infected cells.
The relatively long-lived phagocytic cell of mammalian tissues that are derived from blood MONOCYTES. Main types are PERITONEAL MACROPHAGES; ALVEOLAR MACROPHAGES; HISTIOCYTES; KUPFFER CELLS of the liver; and OSTEOCLASTS. They may further differentiate within chronic inflammatory lesions to EPITHELIOID CELLS or may fuse to form FOREIGN BODY GIANT CELLS or LANGHANS GIANT CELLS. (from The Dictionary of Cell Biology, Lackie and Dow, 3rd ed.)
Established cell cultures that have the potential to propagate indefinitely.
The major interferon produced by mitogenically or antigenically stimulated LYMPHOCYTES. It is structurally different from TYPE I INTERFERON and its major activity is immunoregulation. It has been implicated in the expression of CLASS II HISTOCOMPATIBILITY ANTIGENS in cells that do not normally produce them, leading to AUTOIMMUNE DISEASES.
A genus of protozoa parasitic to birds and mammals. T. gondii is one of the most common infectious pathogenic animal parasites of man.
Malaria caused by PLASMODIUM FALCIPARUM. This is the severest form of malaria and is associated with the highest levels of parasites in the blood. This disease is characterized by irregularly recurring febrile paroxysms that in extreme cases occur with acute cerebral, renal, or gastrointestinal manifestations.
Proteins found in any species of bacterium.
A protozoan disease caused in humans by four species of the PLASMODIUM genus: PLASMODIUM FALCIPARUM; PLASMODIUM VIVAX; PLASMODIUM OVALE; and PLASMODIUM MALARIAE; and transmitted by the bite of an infected female mosquito of the genus ANOPHELES. Malaria is endemic in parts of Asia, Africa, Central and South America, Oceania, and certain Caribbean islands. It is characterized by extreme exhaustion associated with paroxysms of high FEVER; SWEATING; shaking CHILLS; and ANEMIA. Malaria in ANIMALS is caused by other species of plasmodia.
Specialized cells of the hematopoietic system that have branch-like extensions. They are found throughout the lymphatic system, and in non-lymphoid tissues such as SKIN and the epithelia of the intestinal, respiratory, and reproductive tracts. They trap and process ANTIGENS, and present them to T-CELLS, thereby stimulating CELL-MEDIATED IMMUNITY. They are different from the non-hematopoietic FOLLICULAR DENDRITIC CELLS, which have a similar morphology and immune system function, but with respect to humoral immunity (ANTIBODY PRODUCTION).
Nonsusceptibility to the invasive or pathogenic effects of foreign microorganisms or to the toxic effect of antigenic substances.
Infections or infestations with parasitic organisms. The infestation may be experimental or veterinary.
Manifestations of the immune response which are mediated by antigen-sensitized T-lymphocytes via lymphokines or direct cytotoxicity. This takes place in the absence of circulating antibody or where antibody plays a subordinate role.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
The larger fragment generated from the cleavage of COMPLEMENT C3 by C3 CONVERTASE. It is a constituent of the ALTERNATIVE PATHWAY C3 CONVERTASE (C3bBb), and COMPLEMENT C5 CONVERTASES in both the classical (C4b2a3b) and the alternative (C3bBb3b) pathway. C3b participates in IMMUNE ADHERENCE REACTION and enhances PHAGOCYTOSIS. It can be inactivated (iC3b) or cleaved by various proteases to yield fragments such as COMPLEMENT C3C; COMPLEMENT C3D; C3e; C3f; and C3g.
Morphologic alteration of small B LYMPHOCYTES or T LYMPHOCYTES in culture into large blast-like cells able to synthesize DNA and RNA and to divide mitotically. It is induced by INTERLEUKINS; MITOGENS such as PHYTOHEMAGGLUTININS, and by specific ANTIGENS. It may also occur in vivo as in GRAFT REJECTION.
The agent of South American trypanosomiasis or CHAGAS DISEASE. Its vertebrate hosts are man and various domestic and wild animals. Insects of several species are vectors.
Protection from an infectious disease agent that is mediated by B- and T- LYMPHOCYTES following exposure to specific antigen, and characterized by IMMUNOLOGIC MEMORY. It can result from either previous infection with that agent or vaccination (IMMUNITY, ACTIVE), or transfer of antibody or lymphocytes from an immune donor (IMMUNIZATION, PASSIVE).
Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake.
Determination of parasite eggs in feces.
The complete genetic complement contained in a set of CHROMOSOMES in a protozoan.
An encapsulated lymphatic organ through which venous blood filters.
The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.
The process by which antigen is presented to lymphocytes in a form they can recognize. This is performed by antigen presenting cells (APCs). Some antigens require processing before they can be recognized. Antigen processing consists of ingestion and partial digestion of the antigen by the APC, followed by presentation of fragments on the cell surface. (From Rosen et al., Dictionary of Immunology, 1989)
Immunoglobulins produced in a response to PROTOZOAN ANTIGENS.
A critical subpopulation of T-lymphocytes involved in the induction of most immunological functions. The HIV virus has selective tropism for the T4 cell which expresses the CD4 phenotypic marker, a receptor for HIV. In fact, the key element in the profound immunosuppression seen in HIV infection is the depletion of this subset of T-lymphocytes.
Deoxyribonucleic acid that makes up the genetic material of protozoa.
A phylum of unicellular parasitic EUKARYOTES characterized by the presence of complex apical organelles generally consisting of a conoid that aids in penetrating host cells, rhoptries that possibly secrete a proteolytic enzyme, and subpellicular microtubules that may be related to motility.
The properties of a pathogen that makes it capable of infecting one or more specific hosts. The pathogen can include PARASITES as well as VIRUSES; BACTERIA; FUNGI; or PLANTS.
A species of trematode blood flukes of the family Schistosomatidae. It is common in the Nile delta. The intermediate host is the planorbid snail. This parasite causes schistosomiasis mansoni and intestinal bilharziasis.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing HEMOGLOBIN whose function is to transport OXYGEN.
The relationships of groups of organisms as reflected by their genetic makeup.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
Cells or feeding stage in the life cycle of sporozoan protozoa. In the malarial parasite, the trophozoite develops from the MEROZOITE and then splits into the SCHIZONT. Trophozoites that are left over from cell division can go on to form gametocytes.
A protozoan parasite of rodents transmitted by the mosquito Anopheles dureni.
The engulfing and degradation of microorganisms; other cells that are dead, dying, or pathogenic; and foreign particles by phagocytic cells (PHAGOCYTES).
Substances elaborated by bacteria that have antigenic activity.
The process of intracellular viral multiplication, consisting of the synthesis of PROTEINS; NUCLEIC ACIDS; and sometimes LIPIDS, and their assembly into a new infectious particle.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
A species of parasitic nematode causing Malayan filariasis and having a distribution centering roughly on the Malay peninsula. The life cycle of B. malayi is similar to that of WUCHERERIA BANCROFTI, except that in most areas the principal mosquito vectors belong to the genus Mansonia.
The restriction of a characteristic behavior, anatomical structure or physical system, such as immune response; metabolic response, or gene or gene variant to the members of one species. It refers to that property which differentiates one species from another but it is also used for phylogenetic levels higher or lower than the species.
Infections or infestations with parasitic organisms. They are often contracted through contact with an intermediate vector, but may occur as the result of direct exposure.
The functional hereditary units of protozoa.
Commonly known as parasitic worms, this group includes the ACANTHOCEPHALA; NEMATODA; and PLATYHELMINTHS. Some authors consider certain species of LEECHES that can become temporarily parasitic as helminths.
Infections of the INTESTINES with PARASITES, commonly involving PARASITIC WORMS. Infections with roundworms (NEMATODE INFECTIONS) and tapeworms (CESTODE INFECTIONS) are also known as HELMINTHIASIS.
An immunoassay utilizing an antibody labeled with an enzyme marker such as horseradish peroxidase. While either the enzyme or the antibody is bound to an immunosorbent substrate, they both retain their biologic activity; the change in enzyme activity as a result of the enzyme-antibody-antigen reaction is proportional to the concentration of the antigen and can be measured spectrophotometrically or with the naked eye. Many variations of the method have been developed.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
Biological activities of viruses and their interactions with the cells they infect.
Bone marrow-derived lymphocytes that possess cytotoxic properties, classically directed against transformed and virus-infected cells. Unlike T CELLS; and B CELLS; NK CELLS are not antigen specific. The cytotoxicity of natural killer cells is determined by the collective signaling of an array of inhibitory and stimulatory CELL SURFACE RECEPTORS. A subset of T-LYMPHOCYTES referred to as NATURAL KILLER T CELLS shares some of the properties of this cell type.
A genus of the family HERPESVIRIDAE, subfamily BETAHERPESVIRINAE, causing infection involving several organs in mice and rats. Murid herpesvirus is the type species.
Glycoproteins found on the membrane or surface of cells.
Any part or derivative of a helminth that elicits an immune reaction. The most commonly seen helminth antigens are those of the schistosomes.
The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.
A negative regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.
The presence of parasites (especially malarial parasites) in the blood. (Dorland, 27th ed)
The theory that T-cells monitor cell surfaces and detect structural changes in the plasma membrane and/or surface antigens of virally or neoplastically transformed cells.
Immunized T-lymphocytes which can directly destroy appropriate target cells. These cytotoxic lymphocytes may be generated in vitro in mixed lymphocyte cultures (MLC), in vivo during a graft-versus-host (GVH) reaction, or after immunization with an allograft, tumor cell or virally transformed or chemically modified target cell. The lytic phenomenon is sometimes referred to as cell-mediated lympholysis (CML). These CD8-positive cells are distinct from NATURAL KILLER CELLS and NATURAL KILLER T-CELLS. There are two effector phenotypes: TC1 and TC2.
Theoretical representations that simulate the behavior or activity of immune system, processes, or phenomena. They include the use of mathematical equations, computers, and other electrical equipment.
A multistage process that includes cloning, physical mapping, subcloning, determination of the DNA SEQUENCE, and information analysis.
A cytokine produced by a variety of cell types, including T-LYMPHOCYTES; MONOCYTES; DENDRITIC CELLS; and EPITHELIAL CELLS that exerts a variety of effects on immunoregulation and INFLAMMATION. Interleukin-10 combines with itself to form a homodimeric molecule that is the biologically active form of the protein.
Proteins found in any species of helminth.
A hemoflagellate subspecies of parasitic protozoa that causes nagana in domestic and game animals in Africa. It apparently does not infect humans. It is transmitted by bites of tsetse flies (Glossina).
A genus of flagellate protozoa comprising several species that are pathogenic for humans. Organisms of this genus have an amastigote and a promastigote stage in their life cycles. As a result of enzymatic studies this single genus has been divided into two subgenera: Leishmania leishmania and Leishmania viannia. Species within the Leishmania leishmania subgenus include: L. aethiopica, L. arabica, L. donovani, L. enrietti, L. gerbilli, L. hertigi, L. infantum, L. major, L. mexicana, and L. tropica. The following species are those that compose the Leishmania viannia subgenus: L. braziliensis, L. guyanensis, L. lainsoni, L. naiffi, and L. shawi.
Agents used in the treatment of malaria. They are usually classified on the basis of their action against plasmodia at different stages in their life cycle in the human. (From AMA, Drug Evaluations Annual, 1992, p1585)
Infections with unicellular organisms formerly members of the subkingdom Protozoa.
A critical subpopulation of regulatory T-lymphocytes involved in MHC Class I-restricted interactions. They include both cytotoxic T-lymphocytes (T-LYMPHOCYTES, CYTOTOXIC) and CD8+ suppressor T-lymphocytes.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.
A subclass of segmented worms comprising the tapeworms.
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
Serum that contains antibodies. It is obtained from an animal that has been immunized either by ANTIGEN injection or infection with microorganisms containing the antigen.
Genotypic differences observed among individuals in a population.
Immunoglobulins produced in response to VIRAL ANTIGENS.
Manipulation of the host's immune system in treatment of disease. It includes both active and passive immunization as well as immunosuppressive therapy to prevent graft rejection.
Class of parasitic flukes consisting of three subclasses, Monogenea, Aspidogastrea, and Digenea. The digenetic trematodes are the only ones found in man. They are endoparasites and require two hosts to complete their life cycle.
An important soluble regulator of the alternative pathway of complement activation (COMPLEMENT ACTIVATION PATHWAY, ALTERNATIVE). It is a 139-kDa glycoprotein expressed by the liver and secreted into the blood. It binds to COMPLEMENT C3B and makes iC3b (inactivated complement 3b) susceptible to cleavage by COMPLEMENT FACTOR I. Complement factor H also inhibits the association of C3b with COMPLEMENT FACTOR B to form the C3bB proenzyme, and promotes the dissociation of Bb from the C3bBb complex (COMPLEMENT C3 CONVERTASE, ALTERNATIVE PATHWAY).
In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships.
A genus of IRIDOVIRIDAE which infects fish, amphibians and reptiles. It is non-pathogenic for its natural host, Rana pipiens, but is lethal for other frogs, toads, turtles and salamanders. Frog virus 3 is the type species.
A genus of the family HERPESVIRIDAE, subfamily BETAHERPESVIRINAE, infecting the salivary glands, liver, spleen, lungs, eyes, and other organs, in which they produce characteristically enlarged cells with intranuclear inclusions. Infection with Cytomegalovirus is also seen as an opportunistic infection in AIDS.
Infections with unicellular organisms formerly members of the subkingdom Protozoa. The infections may be experimental or veterinary.
Infections by nematodes, general or unspecified.
Differentiation antigens residing on mammalian leukocytes. CD stands for cluster of differentiation, which refers to groups of monoclonal antibodies that show similar reactivity with certain subpopulations of antigens of a particular lineage or differentiation stage. The subpopulations of antigens are also known by the same CD designation.
The production of ANTIBODIES by proliferating and differentiated B-LYMPHOCYTES under stimulation by ANTIGENS.
Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment.
A genus of the family HERPESVIRIDAE, subfamily GAMMAHERPESVIRINAE, infecting B-cells in humans and new world primates. The type species human herpesvirus 4 (HERPESVIRUS 4, HUMAN) is better known as the Epstein-Barr virus.
Proteins prepared by recombinant DNA technology.
The phenomenon of target cell destruction by immunologically active effector cells. It may be brought about directly by sensitized T-lymphocytes or by lymphoid or myeloid "killer" cells, or it may be mediated by cytotoxic antibody, cytotoxic factor released by lymphoid cells, or complement.
A family of pattern recognition receptors characterized by an extracellular leucine-rich domain and a cytoplasmic domain that share homology with the INTERLEUKIN 1 RECEPTOR and the DROSOPHILA toll protein. Following pathogen recognition, toll-like receptors recruit and activate a variety of SIGNAL TRANSDUCING ADAPTOR PROTEINS.
The determination of the pattern of genes expressed at the level of GENETIC TRANSCRIPTION, under specific circumstances or in a specific cell.
A parasitic hemoflagellate of the subgenus Leishmania leishmania that infects man and animals and causes cutaneous leishmaniasis (LEISHMANIASIS, CUTANEOUS) of the Old World. Transmission is by Phlebotomus sandflies.
A family of double-stranded DNA viruses infecting mammals (including humans), birds and insects. There are two subfamilies: CHORDOPOXVIRINAE, poxviruses of vertebrates, and ENTOMOPOXVIRINAE, poxviruses of insects.
Virus diseases caused by the HERPESVIRIDAE.
A cell line derived from cultured tumor cells.
The level of protein structure in which combinations of secondary protein structures (alpha helices, beta sheets, loop regions, and motifs) pack together to form folded shapes called domains. Disulfide bridges between cysteines in two different parts of the polypeptide chain along with other interactions between the chains play a role in the formation and stabilization of tertiary structure. Small proteins usually consist of only one domain but larger proteins may contain a number of domains connected by segments of polypeptide chain which lack regular secondary structure.
The degree of similarity between sequences of amino acids. This information is useful for the analyzing genetic relatedness of proteins and species.
A mild, eruptive skin disease of milk cows caused by COWPOX VIRUS, with lesions occurring principally on the udder and teats. Human infection may occur while milking an infected animal.
A genus of the family HERPESVIRIDAE, subfamily GAMMAHERPESVIRINAE, infecting New World primates and other species. HERPESVIRUS 2, SAIMIRIINE is the type species.
Elements of limited time intervals, contributing to particular results or situations.
Lymphoid cells concerned with humoral immunity. They are short-lived cells resembling bursa-derived lymphocytes of birds in their production of immunoglobulin upon appropriate stimulation.
Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
An inhibitory B7 antigen that has specificity for the T-CELL receptor PROGRAMMED CELL DEATH 1 PROTEIN. CD274 antigen provides negative signals that control and inhibit T-cell responses and is found at higher than normal levels on tumor cells, suggesting its potential role in TUMOR IMMUNE EVASION.
An order of heteroxenous protozoa in which the macrogamete and microgamont develop independently. A conoid is usually absent.
Antibodies that reduce or abolish some biological activity of a soluble antigen or infectious agent, usually a virus.
A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.
Infestation of animals with parasitic worms of the helminth class. The infestation may be experimental or veterinary.
An endemic disease that is characterized by the development of single or multiple localized lesions on exposed areas of skin that typically ulcerate. The disease has been divided into Old and New World forms. Old World leishmaniasis is separated into three distinct types according to epidemiology and clinical manifestations and is caused by species of the L. tropica and L. aethiopica complexes as well as by species of the L. major genus. New World leishmaniasis, also called American leishmaniasis, occurs in South and Central America and is caused by species of the L. mexicana or L. braziliensis complexes.
The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes IMMUNE COMPLEX DISEASES.
Antigenic determinants recognized and bound by the T-cell receptor. Epitopes recognized by the T-cell receptor are often located in the inner, unexposed side of the antigen, and become accessible to the T-cell receptors after proteolytic processing of the antigen.
Biologically active substances whose activities affect or play a role in the functioning of the immune system.
Substances that are destructive to protozoans.
Potentially pathogenic bacteria found in nasal membranes, skin, hair follicles, and perineum of warm-blooded animals. They may cause a wide range of infections and intoxications.
An activating NK cell lectin-like receptor subfamily that regulates immune responses to INFECTION and NEOPLASMS. Members of this subfamily generally occur as homodimers.
The type species of LENTIVIRUS and the etiologic agent of AIDS. It is characterized by its cytopathic effect and affinity for the T4-lymphocyte.
Granular leukocytes having a nucleus with three to five lobes connected by slender threads of chromatin, and cytoplasm containing fine inconspicuous granules and stainable by neutral dyes.
CD4-positive T cells that inhibit immunopathology or autoimmune disease in vivo. They inhibit the immune response by influencing the activity of other cell types. Regulatory T-cells include naturally occurring CD4+CD25+ cells, IL-10 secreting Tr1 cells, and Th3 cells.
Serum glycoproteins participating in the host defense mechanism of COMPLEMENT ACTIVATION that creates the COMPLEMENT MEMBRANE ATTACK COMPLEX. Included are glycoproteins in the various pathways of complement activation (CLASSICAL COMPLEMENT PATHWAY; ALTERNATIVE COMPLEMENT PATHWAY; and LECTIN COMPLEMENT PATHWAY).
Endogenous proteins that inhibit or inactivate COMPLEMENT C3B. They include COMPLEMENT FACTOR H and COMPLEMENT FACTOR I (C3b/C4b inactivator). They cleave or promote the cleavage of C3b into inactive fragments, and thus are important in the down-regulation of COMPLEMENT ACTIVATION and its cytolytic sequence.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
A serum protein that regulates the CLASSICAL COMPLEMENT ACTIVATION PATHWAY. It binds as a cofactor to COMPLEMENT FACTOR I which then hydrolyzes the COMPLEMENT C4B in the CLASSICAL PATHWAY C3 CONVERTASE (C4bC2a).
A glycoprotein that is central in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. C3 can be cleaved into COMPLEMENT C3A and COMPLEMENT C3B, spontaneously at low level or by C3 CONVERTASE at high level. The smaller fragment C3a is an ANAPHYLATOXIN and mediator of local inflammatory process. The larger fragment C3b binds with C3 convertase to form C5 convertase.
The arrangement of two or more amino acid or base sequences from an organism or organisms in such a way as to align areas of the sequences sharing common properties. The degree of relatedness or homology between the sequences is predicted computationally or statistically based on weights assigned to the elements aligned between the sequences. This in turn can serve as a potential indicator of the genetic relatedness between the organisms.
A general term for diseases produced by viruses.
A disease caused by any of a number of species of protozoa in the genus LEISHMANIA. There are four major clinical types of this infection: cutaneous (Old and New World) (LEISHMANIASIS, CUTANEOUS), diffuse cutaneous (LEISHMANIASIS, DIFFUSE CUTANEOUS), mucocutaneous (LEISHMANIASIS, MUCOCUTANEOUS), and visceral (LEISHMANIASIS, VISCERAL).
Antibody-mediated immune response. Humoral immunity is brought about by ANTIBODY FORMATION, resulting from TH2 CELLS activating B-LYMPHOCYTES, followed by COMPLEMENT ACTIVATION.
A parasitic hemoflagellate of the subgenus Leishmania leishmania that infects man and animals and causes visceral leishmaniasis (LEISHMANIASIS, VISCERAL). The sandfly genera Phlebotomus and Lutzomyia are the vectors.
A species of PLASMODIUM causing malaria in rodents.
The process of cumulative change at the level of DNA; RNA; and PROTEINS, over successive generations.
Antibodies produced by a single clone of cells.
Lipid-containing polysaccharides which are endotoxins and important group-specific antigens. They are often derived from the cell wall of gram-negative bacteria and induce immunoglobulin secretion. The lipopolysaccharide molecule consists of three parts: LIPID A, core polysaccharide, and O-specific chains (O ANTIGENS). When derived from Escherichia coli, lipopolysaccharides serve as polyclonal B-cell mitogens commonly used in laboratory immunology. (From Dorland, 28th ed)
Serum glycoprotein produced by activated MACROPHAGES and other mammalian MONONUCLEAR LEUKOCYTES. It has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. Also known as TNF-alpha, it is only 30% homologous to TNF-beta (LYMPHOTOXIN), but they share TNF RECEPTORS.
A genus of the family HERPESVIRIDAE, subfamily ALPHAHERPESVIRINAE. Its species include those causing CHICKENPOX and HERPES ZOSTER in humans (HERPESVIRUS 3, HUMAN), as well as several animal viruses.
Transfer of immunity from immunized to non-immune host by administration of serum antibodies, or transplantation of lymphocytes (ADOPTIVE TRANSFER).
Infection with the protozoan parasite TRYPANOSOMA CRUZI, a form of TRYPANOSOMIASIS endemic in Central and South America. It is named after the Brazilian physician Carlos Chagas, who discovered the parasite. Infection by the parasite (positive serologic result only) is distinguished from the clinical manifestations that develop years later, such as destruction of PARASYMPATHETIC GANGLIA; CHAGAS CARDIOMYOPATHY; and dysfunction of the ESOPHAGUS or COLON.
Sites on an antigen that interact with specific antibodies.
Deliberate stimulation of the host's immune response. ACTIVE IMMUNIZATION involves administration of ANTIGENS or IMMUNOLOGIC ADJUVANTS. PASSIVE IMMUNIZATION involves administration of IMMUNE SERA or LYMPHOCYTES or their extracts (e.g., transfer factor, immune RNA) or transplantation of immunocompetent cell producing tissue (thymus or bone marrow).
Proteins isolated from the outer membrane of Gram-negative bacteria.
Substances elaborated by viruses that have antigenic activity.
The study of parasites and PARASITIC DISEASES.
The type species of ORTHOPOXVIRUS, related to COWPOX VIRUS, but whose true origin is unknown. It has been used as a live vaccine against SMALLPOX. It is also used as a vector for inserting foreign DNA into animals. Rabbitpox virus is a subspecies of VACCINIA VIRUS.
Antigens on surfaces of cells, including infectious or foreign cells or viruses. They are usually protein-containing groups on cell membranes or walls and may be isolated.
A genetic rearrangement through loss of segments of DNA or RNA, bringing sequences which are normally separated into close proximity. This deletion may be detected using cytogenetic techniques and can also be inferred from the phenotype, indicating a deletion at one specific locus.
A species of gram-positive, aerobic bacteria that produces TUBERCULOSIS in humans, other primates, CATTLE; DOGS; and some other animals which have contact with humans. Growth tends to be in serpentine, cordlike masses in which the bacilli show a parallel orientation.
Infection with CYTOMEGALOVIRUS, characterized by enlarged cells bearing intranuclear inclusions. Infection may be in almost any organ, but the salivary glands are the most common site in children, as are the lungs in adults.
Immunoglobulins produced in a response to BACTERIAL ANTIGENS.
Serum proteins that negatively regulate the cascade process of COMPLEMENT ACTIVATION. Uncontrolled complement activation and resulting cell lysis is potentially dangerous for the host. The complement system is tightly regulated by inactivators that accelerate the decay of intermediates and certain cell surface receptors.
A species of CERCOPITHECUS containing three subspecies: C. tantalus, C. pygerythrus, and C. sabeus. They are found in the forests and savannah of Africa. The African green monkey (C. pygerythrus) is the natural host of SIMIAN IMMUNODEFICIENCY VIRUS and is used in AIDS research.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
Layers of protein which surround the capsid in animal viruses with tubular nucleocapsids. The envelope consists of an inner layer of lipids and virus specified proteins also called membrane or matrix proteins. The outer layer consists of one or more types of morphological subunits called peplomers which project from the viral envelope; this layer always consists of glycoproteins.
Short sequences (generally about 10 base pairs) of DNA that are complementary to sequences of messenger RNA and allow reverse transcriptases to start copying the adjacent sequences of mRNA. Primers are used extensively in genetic and molecular biology techniques.
Large, phagocytic mononuclear leukocytes produced in the vertebrate BONE MARROW and released into the BLOOD; contain a large, oval or somewhat indented nucleus surrounded by voluminous cytoplasm and numerous organelles.
Culture of an isolated organism free from any other associating or contaminating organisms.
Substances that augment, stimulate, activate, potentiate, or modulate the immune response at either the cellular or humoral level. The classical agents (Freund's adjuvant, BCG, Corynebacterium parvum, et al.) contain bacterial antigens. Some are endogenous (e.g., histamine, interferon, transfer factor, tuftsin, interleukin-1). Their mode of action is either non-specific, resulting in increased immune responsiveness to a wide variety of antigens, or antigen-specific, i.e., affecting a restricted type of immune response to a narrow group of antigens. The therapeutic efficacy of many biological response modifiers is related to their antigen-specific immunoadjuvanticity.
A subfamily of HERPESVIRIDAE characterized by variable reproductive cycles. The genera include: LYMPHOCRYPTOVIRUS and RHADINOVIRUS.
A supergroup (some say phylum) of ameboid EUKARYOTES, comprising ARCHAMOEBAE; LOBOSEA; and MYCETOZOA.
The ability of a pathogenic virus to lie dormant within a cell (latent infection). In eukaryotes, subsequent activation and viral replication is thought to be caused by extracellular stimulation of cellular transcription factors. Latency in bacteriophage is maintained by the expression of virally encoded repressors.
A superfamily of nematodes of the suborder SPIRURINA. Its organisms possess a filiform body and a mouth surrounded by papillae.
Mature LYMPHOCYTES and MONOCYTES transported by the blood to the body's extravascular space. They are morphologically distinguishable from mature granulocytic leukocytes by their large, non-lobed nuclei and lack of coarse, heavily stained cytoplasmic granules.
Serine proteases that cleave COMPLEMENT C3 into COMPLEMENT C3A and COMPLEMENT C3B, or cleave COMPLEMENT C5 into COMPLEMENT C5A and COMPLEMENT C5B. These include the different forms of C3/C5 convertases in the classical and the alternative pathways of COMPLEMENT ACTIVATION. Both cleavages take place at the C-terminal of an ARGININE residue.
Immunoglobulins produced in a response to HELMINTH ANTIGENS.
A classification of T-lymphocytes, especially into helper/inducer, suppressor/effector, and cytotoxic subsets, based on structurally or functionally different populations of cells.
A protozoan parasite that causes vivax malaria (MALARIA, VIVAX). This species is found almost everywhere malaria is endemic and is the only one that has a range extending into the temperate regions.
A genus of DNA viruses in the family PAPILLOMAVIRIDAE, which cause cutaneous lesions in humans. They are histologically distinguishable by intracytoplasmic INCLUSION BODIES which are species specific.
Models used experimentally or theoretically to study molecular shape, electronic properties, or interactions; includes analogous molecules, computer-generated graphics, and mechanical structures.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
Tests that demonstrate the relative effectiveness of chemotherapeutic agents against specific parasites.
The product of meiotic division of zygotes in parasitic protozoa comprising haploid cells. These infective cells invade the host and undergo asexual reproduction producing MEROZOITES (or other forms) and ultimately gametocytes.
Diminished or failed response of an organism, disease or tissue to the intended effectiveness of a chemical or drug. It should be differentiated from DRUG TOLERANCE which is the progressive diminution of the susceptibility of a human or animal to the effects of a drug, as a result of continued administration.
The structure of one molecule that imitates or simulates the structure of a different molecule.
Receptors that are specifically found on the surface of NATURAL KILLER CELLS. They play an important role in regulating the cellular component of INNATE IMMUNITY.
A species in the genus RHADINOVIRUS, subfamily GAMMAHERPESVIRINAE, isolated from patients with AIDS-related and "classical" Kaposi sarcoma.
A genus of flagellate protozoans found in the blood and lymph of vertebrates and invertebrates, both hosts being required to complete the life cycle.
New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms.
Differential and non-random reproduction of different genotypes, operating to alter the gene frequencies within a population.
Large, transmembrane, non-covalently linked glycoproteins (alpha and beta). Both chains can be polymorphic although there is more structural variation in the beta chains. The class II antigens in humans are called HLA-D ANTIGENS and are coded by a gene on chromosome 6. In mice, two genes named IA and IE on chromosome 17 code for the H-2 antigens. The antigens are found on B-lymphocytes, macrophages, epidermal cells, and sperm and are thought to mediate the competence of and cellular cooperation in the immune response. The term IA antigens used to refer only to the proteins encoded by the IA genes in the mouse, but is now used as a generic term for any class II histocompatibility antigen.
The acquired form of infection by Toxoplasma gondii in animals and man.
The process of cumulative change over successive generations through which organisms acquire their distinguishing morphological and physiological characteristics.
Diseases of freshwater, marine, hatchery or aquarium fish. This term includes diseases of both teleosts (true fish) and elasmobranchs (sharks, rays and skates).
A phylum of parasitic worms, closely related to tapeworms and containing two genera: Moniliformis, which sometimes infects man, and Macracanthorhynchus, which infects swine.
It is found to aid the parasite in entering the host cell and in evading an immune response. Cruzipain can help parasites ... Metamorphosis, immune evasion, and adaptation to certain hosts are some of the processes that cruzipain can exert influence ... Cruzipain is involved in aiding the parasite in penetrating and evading the immune response of the host. The cysteine ... of breaking down host tissue and is prepared to signal the escape mechanism if it detects any response from the host's immune ...
... protozoan parasite Toxoplasma gondii has been shown to target IRGs in mice allowing for resistance from the host immune ... involved in important immune defenses against intracellular pathogens and as a result have become a target for immune evasion ... It is possible that IRGs may have existed prior to the Cambrian Explosion as an innate immune mechanism and with the evolution ... 2000). "Pathogen-specific loss of host resistance in mice lacking the IFN-gamma-inducible gene IGTP". Proc Natl Acad Sci U S A ...
Adult and larval worms migrate through the host's blood circulation avoiding the host's immune system. The worms have many ... The life cycle of schistosomes includes two hosts: humans as definitive hosts, where the parasite undergoes sexual reproduction ... tools that help in this evasion, including the tegument, antioxidant proteins, and defenses against host membrane attack ... and allows the parasite to burrow into its host. The parasite's nervous system contains bilobed ganglia and several nerve cords ...
It is thought that these structures, that are derived from hepatocytes including their membranes, aid in the parasites' evasion ... After injection by mosquitoes into the human host, malaria parasites first migrate to liver cells (hepatocytes), where they ... of immune cells known as Kupffer cells that are located in the liver. Sturm, A.; Amino, R.; Van De Sand, C.; Regen, T.; ... Reorganization of Parasite and Host Cell Membranes during Liver Stage Egress". PLoS Pathogens. 7 (9): e1002224. doi:10.1371/ ...
... along with the biochemistry involved in their take-over or evasion of their host's immune system, eventually leading to their ... An extended time is also given on the workings of immunology and how the immune systems of living beings respond to parasite ... Zimmer then discusses a final time the wide variety of parasites that evolved to have humans as their primary hosts and our ... Several chapters are taken to discuss various types of parasites and how they infect and control their hosts, ...
An evasion strategy used by several pathogens to avoid the innate immune system is to hide within the cells of their host (also ... The parasite Trypanosoma brucei uses a similar strategy, constantly switching one type of surface protein for another, allowing ... Finlay BB, McFadden G (February 2006). "Anti-immunology: evasion of the host immune system by bacterial and viral pathogens". ... Immunology covers the study of all aspects of the immune system. The immune system protects its host from infection with ...
... suggesting that they may promote evasion of the host's immune system by preventing the migration of host immune cells. A number ... When secreted, these proteins may modify the host's immune response in order to promote longevity of the parasite. Helminth ... Other helminth proteins promote parasite survival in other ways, particularly since parasites must depend on hosts for the ... Parasites like helminths do not synthesize their own fatty acids or sterols, and are consequently dependent on their hosts for ...
... (alternatively called immune escape or immune evasion) occurs when the immune system of a host, especially of ... African trypanosomes are parasites that are able to escape the immune responses of its host animal through a range of ... Trypanosomes are also able to achieve evasion through the mediation of the host's immune response. Through the conversion of ... For example, the African trypanosome parasites are able to clear the host's antibodies, as well as resist lysis and inhibit ...
Ghosh S, Jiang N, Farr L, Ngobeni R, Moonah S (21 August 2019). "Parasite-Produced MIF Cytokine: Role in Immune Evasion, ... "Leishmania-encoded orthologs of macrophage migration inhibitory factor regulate host immunity to promote parasite persistence ... invasion and immune evasion. A preclinical study showed that blocking parasite MIF improves outcome in severe protozoan ... The circulating MIF binds to CD74 on other immune cells to trigger an acute immune response. Hence, MIF is classified as an ...
VSG allows the trypanosomatid parasites to evade the mammalian host's immune system by extensive antigenic variation. They form ... The properties of the VSG coat that enable immune evasion are: Shielding - the dense nature of the VSG coat (VSG proteins pack ... These proteins allow the parasite to efficiently evade the host animal's immune system. These VSGs allow the organism to ... As T. brucei populations can peak at a size of 1011 within a host this rapid rate of switching ensures that the parasite ...
1] A paratenic host carries the parasite mechanically but no biological change occurs during that carriage Spirocerca lupi is a ... permitting evasion of host responses) have been described in the serum of affected patients.23 There are also cases of ... Other patients may appear to present with polyarthritis (immune-mediated); vague, sometimes severe generalised or localised ... Coprophagous ("dung") beetles are the intermediate hosts, ingesting the eggs which contain the L1 larvae. Within this host, the ...
The tolerance that immune cells normally have to host tissues can be lost, resulting in permanent damage to host cells. Studies ... "Blocking antibody access to neutralizing domains on glycoproteins involved in entry as a novel mechanism of immune evasion by ... While in the merozoite form, malaria parasites invade erythrocytes and reproduce in them. Some blocking antibodies may inhibit ... Blocking antibodies have been described as a mechanism for HSV-1 to evade the immune system. Blocking antibodies can be used in ...
This is part of a complement system evasion strategy that leads to downstream blocking of immune response. In addition, ... has no relation to either the bacteria's virulence or to the host-parasite interaction. Some of the plasmids are necessary for ... Consequently, it is possible for an Ixodes tick to coinfect a host with either two or all other diseases. When a host is ... In response, the host will initiate an inflammatory response to attempt to remove the infection. Borrelia burgdorferi, also, ...
... immune evasion, and establishment of disease in the host. Sepsis caused by gram-negative bacteria is thought to be largely due ... or parasites. Criteria with regard to hemodynamic compromise or respiratory failure are not useful because they present too ... Upon detection of microbial antigens, the host systemic immune system is activated. Immune cells not only recognise pathogen- ... members of the microbiome may not always be an accidental side effect of the deteriorating host immune system. Rather it is ...
Resistance typically protects the host at the expense of the parasite, while tolerance reduces harm to the host without having ... In addition to promoting immune tolerance, other aspects of the microenvironment aid in immune evasion and induction of tumor- ... This process of negative selection ensures that T and B cells that could initiate a potent immune response to the host's own ... Immune tolerance, or immunological tolerance, or immunotolerance, is a state of unresponsiveness of the immune system to ...
With a higher range of outer-membrane proteins, the parasite can evade the immune system of the host more effectively and ... Ehrlichia canis also show evolution in their complex membrane structures and immune evasion strategies. These evolutionary ... The glycoproteins are important targets of the host immune response, attachment to the host cell, and other features in the ... The survival of Ehrlichia depends greatly on the immune response of its host. ...
... by weakening the host's immune system and (ii) by altering the host's cells to be more beneficial to the parasite. The ... Hosts may use behavioral evasion when they encounter an egg laying female parasitoid, like dropping off the plant they are on, ... Some also inject a mix of secretory products that paralyse the host or protect the egg from the host's immune system; these ... causing symptoms that benefit the parasite. Host size is important for the development of the parasitoid, as the host is its ...
Finlay BB, McFadden G. Anti-immunology: evasion of the host immune system by bacterial and viral pathogens. „Cell". 124 (4), s ... Good vs complementary genes for parasite resistance and the evolution of mate choice. „BMC Evol Biol.". 4 (1), s. 48, November ... Fever and reduced iron: their interaction as a host defense response to bacterial infection. „Science". 203 (4378), s. 374-6, ... Virulence is positively selected by transmission success between mammalian hosts. „Curr. Biol.". 17 (9), s. 783-8, May 2007. ...
... several mechanisms of immune evasion by R. seeberi have been identified. A novel method for the determination of the viability ... List of parasites (human) Alexis Berrocal & Alfonso López (March 2007), "Nasal rhinosporidiosis in a mule", Can Vet J, 48 (3): ... Rhinosporidium is generally classified as having a single species, although some evidence indicates that different host species ... Humoral and cell-mediated immune responses in human patients and in experimental mice have been defined; ...
Artavanis-Tsakonas, K; Tongren, JE; Riley, EM (August 2003). "The war between the malaria parasite and the immune system: ... Sturm, A. (2006). "Manipulation of Host Hepatocytes by the Malaria Parasite for Delivery into Liver Sinusoids". Science. 313 ( ... Maurer's cleft and are secretory organelles that produce proteins and enzymes essential for nutrient uptake and immune evasion ... From this stage onward the parasites produce different proteins that help in suppressing communication of the immune cells. ...
The parasite requires two different hosts for a complete life cycle, humans as the definitive host and sandflies as the ... There are two major mechanisms of immune evasion such as induction of immune suppressive IL-10 responses and the generation of ... This protects the parasites from the digestive enzymes of the host. The amastigotes travel as far as the abdominal midgut and ... In this way the amastigotes are able to survive and replicate inside these primary immune systems. The parasites manipulate the ...
Resistance typically protects the host at the expense of the parasite, while tolerance reduces harm to the host without having ... In addition to promoting immune tolerance, other aspects of the microenvironment aid in immune evasion and induction of tumor- ... Immune Tolerance Network International Conference on Immune Tolerance Immune+tolerance at the US National Library of Medicine ... This process of negative selection ensures that T and B cells that could initiate a potent immune response to the host's own ...
Like other Plasmodium parasites, P. knowlesi has a life cycle that requires it be passed back and forth between mammalian hosts ... In 1965 and 1972, several groups characterized how P. knowlesi antigenic variation contributed to immune evasion and chronic ... P. knowlesi has long been used as a research model for studying the interaction between parasite and host, and developing ... which is involved in displaying different antigens on the parasite surface to evade the immune system, and the Kir (knowlesi ...
... the effect on the fitness of a parasite's hosts; the number of hosts they have per life stage; whether the host is prevented ... others introduce a virus which interferes with the host's immune system. Some parasitoid wasps locate hosts by detecting the ... Schmidt, O.; Theopold, U.; Strand, M.R. (2001). "Innate immunity and evasion by insect parasitoids". BioEssays. 23 (4): 344-351 ... Trophically transmitted parasites are transmitted to their definitive host, a predator, when their intermediate host is eaten. ...
... immune evasion, and establishment of disease in the host.[35] Sepsis caused by gram-negative bacteria is thought to be largely ... or parasites.[34] Criteria with regard to hemodynamic compromise or respiratory failure are not useful because they present too ... Host factors[խմբագրել , խմբագրել կոդը]. Upon detection of microbial antigens, the host systemic immune system is activated. ... and to the status of the immune system of the host.[35] The early phase of sepsis characterized by excessive inflammation ( ...
... parasitized host cells which display parasite proteins must be modified to prevent destruction by the host immune defenses. In ... Diamond, MS (2003). "Evasion of innate and adaptive immunity by flaviviruses". Immunology and Cell Biology. 81 (3): 196-206. ... 1993). "Bacterial Antigenic Variation, Host Immune Response, and Pathogen-Host Coevolution". Infection and Immunity. 61 (6): ... the VSG coat is sufficient to protect the parasite from immune detection. The host eventually identifies the VSG as a foreign ...
The protein assists the adhesion and entry of the bacterium into host cells, as well as evasion of the host's immune reaction. ... The parasite first attaches itself to the target cells using surface proteoglycans present on the host cell and bacterial ... Orientia tsutsugamushi has a special adaptation for surviving in the host cell by evading the host immune reaction. Once it ... Chiggers feed only once on a mammalian host. The feeding usually takes 2 to 4 days. In contrast to most parasites, they do not ...
"Immune Evasion by bacteria". Crohnie.. *^ Finlay BB, McFadden G (February 2006). "Anti-immunology: evasion of the host immune ... histamine-releasing basophils are important in the defense against parasites and play a role in allergic reactions, such as ... Immune evasion[edit]. Cells of the innate immune system prevent free growth of microorganisms within the body, but many ... They may also mimick host cells so the immune system does not recognize them as foreign. Staphylococcus aureus inhibits the ...
Roy, Craig R.; Kagan, Jonathan C. (1 January 2013). Evasion of Phagosome Lysosome Fusion and Establishment of a Replicative ... Warr, GW (1997). "The adaptive immune system of fish". Developments in Biological Standardization. 90: 15-21. PMID 9270830.. ... For example, Shigella can secrete toxins that alter the host cytoskeleton and enter the basolateral side of enterocytes.[12] ... such as a parasite.[13] They also deliver various membrane proteins to the phagosome and modify the organelle structure. ...
Coccidians in the genus Aggregata living in the gut cause severe disease to the host. Octopuses have an innate immune system, ... Pathogens and parasites. The diseases and parasites that affect octopuses have been little studied, but cephalopods are known ... The ink is thought to reduce the efficiency of olfactory organs, which would aid evasion from predators that employ smell for ... Pascal, Santiago; Gestal, Camino; Estevez, J.; Arias, Christian Andrés (1996). "Parasites in commercially-exploited cephalopods ...
Host defence mechanisms. See also: Immune system. The body's first line of defence against viruses is the innate immune system ... These persistent viruses evade immune control by sequestration, blockade of antigen presentation, cytokine resistance, evasion ... The virophage as a unique parasite of the giant mimivirus. Nature. 2008;455(7209):100-4. doi:10.1038/nature07218. PMID 18690211 ... The range of host cells that a virus can infect is called its "host range". This can be narrow, meaning a virus is capable of ...
... and it has been proposed that this is important for the establishment of infection and for evasion of the host immune response ... researchers at the University of Oslo in Norway and the University of Ferrara in Italy now believe humans and their parasites ... Like Y. pseudotuberculosis and Y. enterocolitica, Y. pestis is host to the plasmid pCD1. In addition, it also hosts two other ... In humans and other susceptible hostsEdit. Pathogenesis due to Y. pestis infection of mammalian hosts is due to several factors ...
... of malaria-infected red cells This antigen represents critical biological functions for the parasite including immune evasion ... from the intraerythrocytic asexual parasite to the cytoplasmic face of the host cell membrane". The Journal of Cell Biology. ... a parasite protein that this human malaria parasite expresses on the surface ... Howard, RJ (13 November 1984). "Antigenic variation of bloodstage malaria parasites". Philosophical Transactions of the Royal ...
... and this is proposed to be important for the establishment of infection and for evasion of the host immune response. YopO is a ... researchers at the University of Oslo and the University of Ferrara suggested that humans and their parasites were the biggest ... Like Y. pseudotuberculosis and Y. enterocolitica, Y. pestis is host to the plasmid pCD1. It also hosts two other plasmids, ... the plague overall affects the host cell's ability to communicate with the immune system, hindering the body to bring ...
In later stages of a T. brucei infection of a mammalian host the parasite may migrate from the bloodstream to also infect the ... This VSG coat enables an infecting T. brucei population to persistently evade the host's immune system, allowing chronic ... enabling persistent evasion of host adaptive immunity leading to chronic infection. T. brucei is one of only a few pathogens ... Because host immunity against a specific VSG does not develop immediately, some parasites will have switched to an ...
... suggesting that the parasite use this protein for immune evasion by modulating mucosal T cells. Due to their low molecular mass ... increased expression of immunomodulators in Teladorsagia circumcincta larvae derived from host mucosa". Scientific Reports. 7 ( ... MMP-23 may serve as an immune checkpoint to reduce excessive T cell activation during an immune response. In support, increased ... By virtue of suppressing only TEM and TEMRA cells, ShK-186 did not compromise protective immune responses to influenza virus ...
Merl (Matthew James) is a tongue-less Parasite demon with the reputation of a snitch among the underworld community. He hangs ... who are typically immune to telepathy. George is seen reluctantly working for Kr'ph, the demon lord of Westwood in the ... got Spike arrested for tax evasion, and wrote a self-help book that is "a real life-changer." He also supposedly disdains the ... but the process apparently altered her body chemistry to the extent that her host's blood was green. Her ambition is to become ...
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Proteases are a ubiquitous group of enzymes that play key roles in the life cycle of parasites, in the host-parasite ... The oligopeptidase B of Leishmania regulates parasite enolase and immune evasion.. Swenerton RK1, Zhang S, Sajid M, ... In a wild type infection, surface enolase (black diamonds) binds host plasminogen (dark gray circles) on the parasite cell ... Whereas wild type parasites elicited little, if any, response from infected macrophages, OPB(-/-) parasites induced a massive ...
... strategies for immune evasion; STAT signalling; parasite modulation of toll-like receptors in macrophages; T cells in ... Topics covered include: modulation of host miRNA; heat shock proteins; Iron in the Leishmania-macrophage interaction; oxidative ... and a host of other content that defies easy categorization. We help people distribute information and art spanning a wide ...
... possibly because the organism has co-evolved with its many vertebrate hosts and has developed multiple strategies to persist ... Toxoplasma gondii is a common parasite of animals and humans and can cause serious opportunistic infections. However, the ... Host-Parasite Interactions* * Humans * Immune Evasion * Immunity, Innate* * Mice * Protein-Tyrosine Kinases / genetics ... Toxoplasma gondii is a common parasite of animals and humans and can cause serious opportunistic infections. However, the ...
... once an obscure protozoan parasite, has recently become the focus of intense research, both as a serious pathogen in its own ... Mechanisms of Immune Evasion 8. Apoptosis and its Impact on the Parasite-Host Interaction 9. Pathogenicity and Virulence in ... Dense Granules of the Infectious Stages of Toxoplasma gondii: Their Central Role in the Host/Parasite Relationship 26. Calcium ... The Toxoplasma gondii Parasitophorous Vacuole Membrane: Transactions at the Parasite Host Interface ...
how do immune-mediated host-parasite interactions affect parasite fitness? (protective immunity vs. parasite immune evasion) ... I study how parasitic helminths are affected by host immune responses as a function of parasite immune evasion and immune ... anti-filarial vaccines that target parasite immune modulators and thus limit the ability of these worms to evade host immune ... Filarial Parasites Develop Faster and Reproduce Earlier in Response to Host Immune Effectors Which Determine Filarial Life ...
Immune Recognition and Evasion: Molecular Aspects of Hostparasite Interaction. RICHARD A. YOUNG ... News Feature: Do hosts and their microbes evolve as a unit?. A group of evolutionary biologists sees evidence for a hologenome ... Type VI secretion system contributes to Enterohemorrhagic Escherichia coli virulence by secreting catalase against host ... Stress proteins and the immune response to mycobacteria ? Antigens as virulence factors? ...
Project Understanding immune evasion by malaria parasites Researcher (PI) Ron Dzikowski Host Institution (HI) THE HEBREW ... Its virulence is attributed to its ability to evade the human immune system, by modifying the host red blood cell surface to ... Its virulence is attributed to its ability to evade the human immune system, by modifying the host red blood cell surface to ... The expected outcome of this knowledge is new concepts for disrupting the parasites ability to evade immune attack which will ...
Immunity to and immune evasion by bacteria, viruses and parasites *Vaccine and adjuvant development ... T cell biology and role of T cell subtypes in regulating host immune responses ... bacteria and parasites and also functions in protection against cancer. The immune system uses innate and adaptive (T and B ... evasion of immunity by pathogens, infectious disease and cancer vaccines and the genetic basis of immune- mediated diseases, ...
... highly effective approaches for immune evasion. Originally developed for protection against host immune responses, viral immune ... Despite this, the use of virus-derived proteins as natural sources for immune modulators remains in the early stages of ... These complex viral intracellular parasites have "performed the R&D", developing highly effective immune evasive strategies ... highly effective approaches for immune evasion. Originally developed for protection against host immune responses, viral immune ...
These receptors function in cell adhesion, entry into host cells, and immune system evasion. Due to their accessibility on the ... We have solved the structure of the two domains anchored to the parasite membrane at the end of the invasion process. Host ... surface of the parasite and their functional importance, many show promise as vaccine candidates. We have solved the structure ... As a requirement for invasion into the red cell of a mammalian host, MSP-1 undergoes two proteolytic processing stages. ...
Malaria parasites have evolved ingenious mechanisms to escape the human immune system to enable the establishment of successful ... Malaria parasites have evolved ingenious mechanisms to escape the human immune system to enable the establishment of successful ... Recent studies identifying novel host-pathogen interactions between the complement system and malaria parasites yield insights ... Plasmodium Malaria Merozoite Surface proteins Complement evasion Factor H 6 Cysteine proteins Parasite invasion ...
... some parasites live inside the cells of the host so theyre essentially not seen by the immune system; and some parasites will ... Essentially its down to a very sophisticated array of evasion strategies. Some parasites will coat themselves with the ... subvert the immune system of the host to the parasites advantage.. Chris - But havent some people said that thats really ... Lots of parasites certainly are a big problem. Nowadays theres certainly a change in peoples thinking in that some parasites ...
Parasite Immune Evasion and Manipulation of Host Phenotype ; 9. Infection and Pathogenesis ; 10. Host-Parasite Genetics ; 11. ... Host-Parasite (Co-)Evolution ; 14. Parasites and Host Ecology ; Glossary ; Immunological Acronyms ; References ; Index ... His current research focuses on host-parasite interactions and co-evolution, maintenance of genetic diversity, recombination, ... The Diversity and Natural History of Parasites ; 4. The Natural History of Defences ; 5. Ecological Immunology ; 6. Parasites, ...
Herpes virus immune evasion via non-coding RNA regulatory elements. Sing Sing Way, M.D., Ph.D.. University of Minnesota Medical ... TLR-independent host resistance to protozoan parasites. Liang Zhou, M.D., Ph.D.. Northwestern University. Environmental impact ... Innate immune regulation of host-microbe interaction. Peter J. Turnbaugh, Ph.D.. University of California-San Francisco. Kochs ... Novel RNAi-like system controls bacterial innate immune evasion and virulence. Felix Yarovinsky, M.D.. University of Texas ...
It is found to aid the parasite in entering the host cell and in evading an immune response. Cruzipain can help parasites ... Metamorphosis, immune evasion, and adaptation to certain hosts are some of the processes that cruzipain can exert influence ... Cruzipain is involved in aiding the parasite in penetrating and evading the immune response of the host. The cysteine ... of breaking down host tissue and is prepared to signal the escape mechanism if it detects any response from the hosts immune ...
... creating a dynamic interaction between the human immune system and the parasite population. ... But new techniques are starting to expose the diverse mechanisms by which these agents modulate or evade their hosts defences ... Immunological modulation and evasion by helminth parasites in human populations.. Maizels RM1, Bundy DA, Selkirk ME, Smith DF, ... Helminth parasites are highly prevalent in human communities in developing countries. In an endemic area an infected individual ...
Using RT-PCR and western blot, sequences related to progesterone receptor were detected in the parasite. A phylogenetic ... possibly through its binding to a progesterone receptor synthesized by the parasite. ... R. T. Damian, "Parasite immune evasion and exploitation: reflections and projections," Parasitology, vol. 115, supplement, pp. ... "Neuroimmunoendocrine modulation in the host by helminth parasites: a novel form of host-parasite coevolution?" ...
R. T. Damian, "Parasite immune evasion and exploitation: reflections and projections," Parasitology, vol. 115, supplement, pp. ... "Neuroimmunoendocrine modulation in the host by helminth parasites: a novel form of host-parasite coevolution?" ... Progesterone Induces Scolex Evagination of the Human Parasite Taenia solium: Evolutionary Implications to the Host-Parasite ... "Parasite regulation by host hormones: an old mechanism of host exploitation?" Trends in Parasitology, vol. 21, no. 12, pp. 588- ...
His work concentrates on the interaction between parasites and their host`s immune system. He is bearer of the Leuckart medal ... 1.6.2 Immune Evasion 68. 1.6.3 Parasites as Opportunistic Pathogens 72 ... 1.3 The Impact of Parasites on Host Individuals and Host Populations 30 ... His research has focused on immune responses to parasites, especially intestinal nematodes. He was awarded the Wright Medal ...
... inhibiting immune responses by favoring immune cell apoptosis. Secondly, exosomes play anti-infection roles through: (1) ... inhibiting immune responses by favoring immune cell apoptosis. Secondly, exosomes play anti-infection roles through: (1) ... inhibiting pathogen proliferation and infection directly; (2) inducing immune responses such as those related to the function ... inhibiting pathogen proliferation and infection directly; (2) inducing immune responses such as those related to the function ...
Her group discovered the important role that parasite surface proteins play in immune evasion strategies; the discovery of ... Wai-Hongs research explores the mechanisms regulating successful infection of malaria parasites within the human host. Her ... She has also identified parasite proteins that bind to human immune regulators to subvert the human immune system for parasite ... Her work focuses on deciphering the immune system with genomics and bioinformatics approaches. She co-chairs the international ...
... and on the expression of the virulence factors involved in the immune evasion mechanisms of the host and on the pathogenesis of ... These details are determinant in the equilibrium of the pathogen-host interaction and the result of this relation, which can ... The current issue highlights the research on subversion and modulation of host defense mechanisms associated with the ... Parasites Kinetoplastids cause a number of serious diseases that have contributed to death and health problems in humans. The ...
... protozoan parasite Toxoplasma gondii has been shown to target IRGs in mice allowing for resistance from the host immune ... involved in important immune defenses against intracellular pathogens and as a result have become a target for immune evasion ... It is possible that IRGs may have existed prior to the Cambrian Explosion as an innate immune mechanism and with the evolution ... 2000). "Pathogen-specific loss of host resistance in mice lacking the IFN-gamma-inducible gene IGTP". Proc Natl Acad Sci U S A ...
Hosts, in turn, have evolved complex defences, with immune systems being among the most sophisticated processes known in nature ... In response, parasites have again found ways to manipulate and exploit their hosts. ... They affect almost every aspect imaginable in the life of their hosts, even as far as the structure of entire ecosystems. ... Parasites and infectious diseases are everywhere and represent some of the most potent forces shaping the natural world. ...
In addition, recent evidence suggests that the parasites use oxylipins to evade the hosts immune system. A generalized immune ... These studies suggest a novel mechanism for parasite evasion of immune responses. ... with parasites surviving for long periods of time in host tissues. The strategies used by the parasites to evade the immune ... This indicates a role for parasite enzymes in host eicosanoid production and a role for host eicosanoids in parasite ...
Researchers discover immune evasion strategy used by Malaria-causing parasite More information: Metabolome modulation of the ... Little is known about parasite interactions with the immune system in a living host, especially in children who are the most ... Researchers discover immune evasion strategy used by Malaria-causing parasite. Oct 09, 2020 ... Latest data on immune response to COVID-19 reinforces need for vaccination. Jun 18, 2021 ...
Rapid and sensitive detection and identification of Plasmodium parasites is crucial for treating patients and mo...... ... PIMMS43 is required for malaria parasite immune evasion and sporogonic development in the mosquito vector Microbiology ... and before they can reach the mosquito salivary glands to be transmitted to a new host, Plasmodium parasites must establish an ... Source: Parasites and Vectors - March 30, 2020. Category: Microbiology Authors: Sinnathamby N. Surendran, Tibutius T. P. ...
Communication between Toxoplasma gondii and its host: impact on parasite growth, development, immune evasion, and virulence. ... Host and parasite-derived IKK activities direct distinct temporal phases of NF-kappaB activation and target gene expression ... MYD88; MYD88 innate immune signal transduction adaptor [KO:K04729]. 3654 IRAK1; interleukin 1 receptor associated kinase 1 [KO: ... Direct activation of STAT3 by the parasite enhance anti-inflammatory function of IL-10 and TGF beta. T. gondii can cause ...
... mucin and MASP expression and how their genetic and antigenic diversification contributes to parasite immune evasion and host ... expression and to investigate the function of antigenic diversification in parasite-host cell interaction and immune evasion. 3 ... hypervariable regions and produce highly O-glycosylated proteins that are potentially involved in host immune evasion and host ... Current Research Our laboratory is interested in the molecular mechanisms by which pathogens evade the host immune system to ...
  • Essential reading for all researchers working with Toxoplasma and related apicomplexans, Plasmodium, Cryptosporidium, and other protozoan parasites. (
  • Malarial surface proteins: Through the course of its life cycle, the malaria parasite Plasmodium expresses scores of receptors on its surface. (
  • The team studied blood samples from children from two ethnic groups in remote rural areas of Burkina Faso, Gouin and Fulani, to see how they responded to the malaria parasite Plasmodium falciparum. (
  • Rapid and sensitive detection and identification of Plasmodium parasites is crucial for treating patients and mo. (
  • After being ingested by a female Anopheles mosquito during a bloodmeal on an infected host, and before they can reach the mosquito salivary glands to be transmitted to a new host, Plasmodium parasites must establish an infection of the mosquito midgut in the form of oocysts. (
  • The human malaria parasite Plasmodium falciparum survives pressures from the host immune system and antimalarial drugs by modifying its genome. (
  • Plasmodium falciparum is the deadliest malaria parasite species, accounting for the vast majority of disease cases and deaths. (
  • Genetic mapping is a powerful method to identify mutations that cause drug resistance and other phenotypic changes in the human malaria parasite Plasmodium falciparum . (
  • Unlike many pathogens I discuss on here, Plasmodium is a protozoan--a eukaroyte with a nucleus, like you and I. It also has a very complex life cycle, going through different stages in its mosquito and vertebrate host. (
  • Not only can an individual be infected with different species of Plasmodium , but the parasite can switch the antigens it presents--the proteins on the parasite surface that the immune system recognizes. (
  • The scientific paper analyzing the genome of that parasite, Plasmodium falciparum, is being published this week in the journal Nature along with a comparison of the genome to the genetic sequence of a rodent malaria parasite, P. yoelii yoelii, which is used as a model to study the human form of the disease. (
  • and Anaplasma marginale (among bacteria) and African trypanosomes, Plasmodium falciparum, and Babesia bovis (among parasites) are examples of pathogens using these mechanisms. (
  • Selection of Plasmodium falciparum Parasites for Cytoadhesion to Human Brain Endothelial Cells Antoine Claessens 1 , J. Alexandra Rowe 1 1 Centre for Immunity, Infection and Evolution, University of Edinburgh An in vitro model for cerebral malaria sequestration is described 1 . (
  • Heterochromatin in the chromososome ends (telomers) in the malarial parasites mediate epigenetic regulation in the malaria parasite Plasmodium falciparum . (
  • Cui L and Miao J (2010) Chromatin‐mediated epigenetic regulation in the malaria parasite Plasmodium falciparum. (
  • It is also the most common target of the PfEMP1 proteins of the malaria parasite, Plasmodium falciparum , tethering parasite-infected erythrocytes to endothelial receptors. (
  • However, with the idea of gene expression in Plasmodia where P. recent availability of the genomes of the human host, f alciparum poses specific experimental the parasite (3D7 clone of Plasmodium difficulties[7, 8]. (
  • C) Activity against parasites/protozoa Both the Bothrops brazili crude venom and its metalloproteinase (BbMP-1) are act against Plasmodium falciparum in vitro and showed low IC50 levels (0.17 and 3.2 mg/mL respectively) 71. (
  • Plasmodium falciparum invasion protein EBA-175, once shed from the parasite surface post invasion, facilitates RBC clustering and enhances parasite growth while simultaneously enabling parasite immune evasion of host neutralizing antibodies. (
  • Epigenetic landscapes underlining global patterns of gene expression in the human malaria parasite, Plasmodium falciparum. (
  • Plasmodium falciparum parasites remodel the surface of human erythrocytes on invasion by the insertion of parasite-derived proteins in knob-like protrusions. (
  • how do immune-mediated host-parasite interactions affect parasite fitness? (
  • Recent studies identifying novel host-pathogen interactions between the complement system and malaria parasites yield insights on the mechanisms of parasite entry into red blood cells, complement evasion strategies and the development of malaria pathogenesis. (
  • Antibody-receptor interactions: Fc receptors are found on the surface of immune cells, where they couple the exact specificity of antibodies to the specialized effector functions of different immune cells. (
  • His current research focuses on host-parasite interactions and co-evolution, maintenance of genetic diversity, recombination, social systems, immune defence strategies, and ecological immunology. (
  • Today, concepts borrowed from evolution, ecology, parasitology, and immunology have formed a new synthesis for the study of host-parasite interactions. (
  • Little is known about parasite interactions with the immune system in a living host, especially in children who are the most vulnerable age group to the infection. (
  • Common areas include mechanisms of host immunity and analysis of complex host-pathogen interactions such as determinants of virulence and immune evasion mechanisms. (
  • Topics have included aquatic food chain energetics, host-parasite and plant/animal interactions, gene expression, and molecular mechanisms of vertebrate development. (
  • The coevolutionary dynamics can be driven by negative frequency-dependent selection, leading to the maintenance of allelic diversity at genes involved in interactions between hosts and pathogens [4] - [7] . (
  • Students will learn basic principles of host-parasite interactions with focus on some pathological properties and examples of particular pathogens that play an important role in major human diseases. (
  • The Smith Lab is interested in understanding the molecular mechanisms governing parasite-vessel wall interactions. (
  • We investigate the structure and function of PfEMP1 proteins and host receptor interactions associated with deadly malaria complications. (
  • We are also working with collaborators at the University of Washington Department of Bioengineering to develop better in vitro endothelial models to study parasite-host vessel wall interactions and characterize malaria vascular disease mechanisms. (
  • Other species are purpose of host-parasite interactions is to identify not that A-T rich. (
  • Molecular Aspects of Host-Parasite Interactions in Malaria: A Brief Review carries genes for 25 tRNAs which have unique prove more suitable for development as MSP-1- features, including the presence of an intron in one of based vaccines than the naturally-occurring them[12]. (
  • For the first time, this book gives a comprehensive overview over the many facets of host-parasite interactions, from the molecular bases to individual strategies and to the ecological and evolutionary consequences. (
  • To gain more insight into the biology of T. vivax , its interactions with the host and consequently its pathogenesis, we have developed a number of reproducible murine models using a parasite isolate that is infectious for rodents. (
  • In order to circumvent the major constraints inherent to studying T. vivax /host interactions in the field, we developed in vivo murine models of T. vivax trypanosomosis. (
  • The effects of the ME on the parasite-host interactions appeared to be mouse strain-dependent, but also related to the ripening stage of the neem fruits, as only the unripe fruit seed kernel extracts displayed appreciable bioactivity. (
  • Interactions of the mermithid nematode Romanomermis culicivorax with the immune system of mosquito larvae were examined by scanning electron microscopy. (
  • The 'extracellular region' that corresponds to allergen V5/Tpx-1 related, considered important in parasite-host interactions, was also identified. (
  • Our work is a significant breakthrough in the field as it should lead, in the future, to the identification of parasite genes that are relevant to its biology and fate, and to work that may shed light on the intricacies of T. vivax- host interactions. (
  • Mononuclear phagocytes and other leukocytes are thought to be responsible for both initiation of graft-versus-host reaction and for the subsequent injury to host tissues after complex interactions with cytokines and chemokines ( 1 , 2 , 7 - 9 ). (
  • On a fundamental level, we elucidate transcriptional alterations taking place throughout the life cycle, characterize the parasite's gene silencing machinery, and explore molecules involved in development, reproduction, host-parasite interactions, immunity, and disease. (
  • The secretome of H. contortus is particularly rich in peptidases linked to blood-feeding activity and interactions with host tissues, and a diverse array of molecules is involved in complex immune responses. (
  • This paper reviews the principles of proteomics, as well as its key instruments and research applications in helminthology, including host parasite interactions, vaccine development and diagnosis of liver fluke diseases and encourage more young researchers to initiate work on the molecular aspects of these economically cosmopolitan parasites. (
  • It has underpinned malaria discoveries relating to host-pathogen interactions, the immune response and immune evasion strategies. (
  • However, due to discrepancies in both innate and adaptive immunity between mice and men the evaluation of the vaccinia virus' interactions with the host immune system in mice are not fully conclusive of what is actually happening in human cancer patients after systemic administration of vaccinia virus. (
  • Therefore, a good in vivo model for testing interactions between vaccinia virus and human immune cells, avoiding the numerous limitations and risks associated with human studies, could be a humanized mouse model. (
  • In addition we exploit the relative susceptibility of ITT sheep to temperate fasciolosis ( Fasciola hepatica ∈dex Fasciola hepatica ) to contrast parasite-host interactions and identify parasite immune evasion strategies to boost the discovery of new vaccine candidates and effector pathways, which may be amenable to exogenous control. (
  • Although this undoubtedly affects their interactions with the host, any effects on immune evasion are at present unknown. (
  • Mechanisms of Immune Evasion 8. (
  • I am interested in the mechanisms that underlie protective immunity and disease: the phenotypes immune cells adopt to mitigate disease, and how to detect and quantify protective immune profiles in laboratory models, domesticated animals, and in natural populations. (
  • The immune system uses innate and adaptive (T and B cells) defence mechanisms to recognize and respond to foreign antigens on pathogens. (
  • Malaria parasites have evolved ingenious mechanisms to escape the human immune system to enable the establishment of successful blood-stage infection. (
  • But new techniques are starting to expose the diverse mechanisms by which these agents modulate or evade their hosts' defences, creating a dynamic interaction between the human immune system and the parasite population. (
  • The severity of these infections depends in most cases on the nature of the pathogen, on its different degrees of propagation, and on the expression of the virulence factors involved in the immune evasion mechanisms of the host and on the pathogenesis of infection. (
  • The objective of this Research Topic is to evaluate the immunological cellular and humoral mechanisms developed by vertebrate hosts and consequently the escape routes that these pathogenic trypanosomatids developed to deceive and escape from protective imune responses. (
  • The current issue highlights the research on subversion and modulation of host defense mechanisms associated with the immunopathogenesis of trypanosomatid infections, providing a broad survey of issues in this field. (
  • He obtained his BS degree in biology with a specialty in genetics, and MSc and PhD degrees in molecular and cellular biology studying the mechanisms of complement system evasion by trypanosomes. (
  • Our laboratory is interested in the molecular mechanisms by which pathogens evade the host immune system to establish infection. (
  • We are interested in understanding the molecular mechanisms that control mucin and MASP expression and how their genetic and antigenic diversification contributes to parasite immune evasion and host cell interaction. (
  • We use CRISPR-Cas9 technology and single cell analysis to understand the transcriptional and post-transcriptional mechanisms that control mucin and MASP gene expression and to investigate the function of antigenic diversification in parasite-host cell interaction and immune evasion. (
  • There is a credible but uncertain basis for hope that effective therapeutic vaccines may be developed eventually, because the healthy immune system can and does cure most infections in the normal recovery processes, mainly through cell-mediated immune mechanisms. (
  • The mechanisms for infection, proliferation, and persistence of viruses in cells of the permissive host are the means by which these genetic entities preserve their specificity and identity in perpetuity. (
  • Pathogens have evolved elegant mechanisms to acquire essential nutrients from host environments. (
  • Genetic recombination and nucleotide substitution are the two major mechanisms that the parasite employs to generate genome diversity. (
  • A better understanding of these mechanisms may provide important information for studying parasite evolution, immune evasion and drug resistance. (
  • A better understanding of the molecular mechanisms of drug resistance, the molecular basis of the host immune response, and the strategies the parasite employs to evade host immunity is critical for vaccine and drug development. (
  • The principles of hypersensitivity, allergic and anaphylactic reactions and other immunopathologic mechanisms (acquired disorders of immune deficiency, auto-immunity and auto-immune diseases). (
  • Mechanisms of disease development and evasion mechanisms employed by the parasites in response to the activated immune mechanisms. (
  • Explain The Principles Of Hypersensitivity, Allergic And Anaphylactic Reactions And Other Immunopathologic Mechanisms (Acquired Disorders Of Immune Deficiency, Auto-Immunity And Auto-Immune Diseases) And Means To Regulate Disease Activity By Pharmacological And Biological Agents. (
  • Through the understanding of the growing variety of mechanisms of the antigenic variation of surface proteins, it has become possible for us to determine what is preventing the host organism from mounting an effective immune response. (
  • A major research interest for the Smith Lab is to decipher how infected red blood cells attach to different microvascular beds and understanding vascular disease mechanisms caused by sequestered parasites. (
  • The organization of parasite genomes and some of the unique mechanisms of mRNA editing found in parasites will also be covered. (
  • Patterns in the distribution of parasites will be described and the mechanisms responsible for generating those patterns evaluated. (
  • There is a close relationship between hormones, cytokines, neuropeptides, and neurotransmitters that modulate the host immune response by several effector mechanisms, including both cellular and humoral immunity. (
  • Thus, understanding the mechanisms involved in immunoendocrine modulation and its effects on parasites is essential for developing new drugs, finding vaccine targets and devising new therapies for several infectious diseases. (
  • This is an advance in the knowledge of host-parasite relationship that contributes to the understanding of host immune response and theileriosis evasion mechanisms. (
  • Understanding mechanisms by which such parasites evade immune or chemotherapeutic elimination is required for development of effective vaccines or drug treatments. (
  • Malaria organism is a highly successful parasite parasites are sometimes easier to clone and express with very sophisticated mechanisms for survival in as soluble proteins are therefore used to get some the host's hostile environment. (
  • More than reflecting only the main parasitological parameters of the animal infection, the mouse model can be used to elucidate the immunopathological mechanisms involved in parasite evasion and persistence, and the tissue damage seen during infection and disease. (
  • The establishment of T. cruzi infection depends on a number of factors that begins with the invasion of host cells, which mobilizes various effector mechanisms of the immune system, such as the activation of factors related to innate immunity and acquired immunity. (
  • This research paper aims to answer what are the types of immune response used by the infected host during the developmental stages of the parasite, as well as what are the possible evasion mechanisms used by the T. cruzi that allows its survival in a hostile environment created by the response of the host immune system. (
  • In an effort to develop anti-leishmaniasis vaccines and adjuvants, novel carbohydrate-based probes were made to study the mechanisms of immune modulation. (
  • We conclude that stage-specific expression of SRS Ags is among the key mechanisms by which optimal parasite persistency is established and maintained. (
  • This accumulating knowledge helps us better understand evasion mechanisms employed by promastigotes and/or amastigotes of Leishmania which could help in the development of more efficient anti-leishmanial therapies in the near future. (
  • Identifying these manipulation factors, via associating gene expression shifts in the parasite with behavioural changes in the host and following their effects will provide researchers with a bottom-up approach to unraveling the mechanisms of behavioural manipulation and by extension behaviour itself. (
  • The mechanisms by which Toxoplasma grows within its host cell, encysts, and interacts with the host's immune system are important questions. (
  • These technologies and approaches have been instrumental in increasing our understanding of Toxoplasma replication within its host cell, bradyzoite development, and virulence mechanisms. (
  • One of the hallmarks of kinetoplastid parasites is their evasion mechanisms from host immunity, leading to disease chronification. (
  • Lectures will cover different parasites at the molecular, cellular and population level concentrating on the active areas of contemporary research such as malaria vaccines, hookworm vaccines, the mechanisms underlying chronic parasite infections and the debilitating pathology caused by for example filariasis and schistosomiasis. (
  • Among different species, at least four mechanisms are known that could facilitate evasion of the host immune response, although no one species is (yet) known to use them all. (
  • We understand very little about the mechanisms used by these parasites to survive. (
  • Consequently, vaccines and mechanisms of immune protection have been studied quite thoroughly. (
  • Additionally, these OPB(-/-) parasites displayed decreased virulence in the murine footpad infection model. (
  • Over the past two decades, infection studies in the mouse, combined with forward-genetics approaches aimed at unravelling the molecular basis of infection, have revealed that T. gondii virulence is mediated, in part, by secretion of effector proteins into the host cell during invasion. (
  • Pleural cellular reaction to the filarial infection Litomosoides sigmodontis is determined by the moulting process, the worm alteration, and the host strain. (
  • The combined strengths in immunology, inflammation and Infection are critical in developing an understanding of the pathogenesis of infectious diseases, immune mediated diseases and cancer. (
  • The following provides a brief overview of complement evasion strategies employed by blood-stage malaria parasites and highlights the importance of understanding the complex interplay between complement and parasite infection. (
  • Host antibodies against these two domains confer protection against malaria infection. (
  • By combining the DNA of cruzipain and chagasin to synthesize a vaccine, a balanced immune response that decreases blood and tissue parasites, as well as the tissue damage caused by Trypanosoma cruzi infection can be induced. (
  • Recent information reveals that sex hormones can affect the course of a parasite infection [ 12 - 16 ], as in the case of taeniasis/cysticercosis [ 17 - 19 ]. (
  • Thus, eicosanoids and oxylipins (host or microbe) may be mediators of a direct host-pathogen "cross-talk" that promotes chronic infection and hypersensitivity disease, common features of infection by eukaryotic pathogens. (
  • Using diverse sources to present a model of why these microbes produce oxylipins, we will also present evidence that these microbial oxylipins may play a significant role in a host-pathogen "cross-talk" that contributes to chronic infection. (
  • Studying the enigmatic, less-malaria-susceptible Fulani ethnic group revealed opposing steroid profiles and stronger immune reactivity to infection. (
  • T. gondii can cause lifelong chronic infection by establishing an anti-apoptotic environment through induction of bcl-2 or IAPs and by redirecting LDL-mediated cholesterol transport to scavenge nutrients from the host. (
  • Paradoxically, these same pathways are utilized during infection by distinct intracellular microorganisms in order to evade recognition by the immune system, inhibit apoptosis, and therefore survive, reproduce, and develop inside cells. (
  • Knowledge of the very complex composition and function of the innate and adaptive branches of the immune system is essential to understanding persistent infection. (
  • One is hit and run infection whereby there is successive propagation in a series of hosts. (
  • The most common resolution of viral infection is by an effective cell-mediated immune response, requiring the virus to escape to new hosts before immunological resolution or before death of the host itself. (
  • Genetic manipulation of both host and pathogen is a feature of many strands of research, in addition to application of state of the art imaging technologies to investigate both cellular events and infection in vivo. (
  • Herpes simplex virus 1 (HSV-1) is a human pathogen that persists for the lifetime of the host as a result of its ability to establish latent infection within sensory neurons. (
  • Analysis of var gene expression in placental parasites from primigravid women in Malawi did not support a role for this conserved gene in placental infection but identified a second commonly occurring var gene. (
  • Principles of chemotherapy in infections and infectious diseases The principles of interaction between host immune responses and establishment of infection. (
  • Discuss The Interaction Between Host Immune Responses And The Establishment Of Infection. (
  • Nevertheless, despite this extensive organismal complexity, in the majority of cases the immune responses of the hosts to worm infection are remarkably similar, being Th2-like with the production of significant quantities of interleukin-4 (IL-4), IL-5, IL-9, IL-10, and IL-13 and consequently the development of strong immunoglobulin E (IgE), eosinophil, and mast cell responses. (
  • The host-protective nature of these lesions has been demonstrated by work in a mouse model of infection with the human parasite. (
  • Although acquired immunity limits the clinical impact of infection and provides protection against parasite replication, experimental evidence indicates that cell-mediated immune responses also result in detrimental inflammation and contribute to the aetiology of severe disease. (
  • Thus, an appropriate regulatory balance between protective immune responses and immune-mediated pathology is required for a favourable outcome of infection. (
  • Control of infection is the main function of the immune system. (
  • Sex hormones play an influential role in the control of parasitic infection by modulating different components of both the innate and adaptive immune responses. (
  • Tick-transmitted single-cell parasites of the phylum Apicomplexa cause disease and result in death or persistent infection and represent a major challenge to global human and animal health. (
  • Therefore, comparison of the T. equi DNA genome to closely related parasites was undertaken to: 1) identify genes contributing to immune evasion and persistence in the horse host, 2) identify genes involved in the infection of horse white blood cells, and 3) determine the relative position of the T. equi organism compared to similarly DNA genome sequenced apicomplexan parasites. (
  • Transmission of arthropod-borne apicomplexan parasites that cause disease and result in death or persistent infection represents a major challenge to global human and animal health. (
  • Therefore comparative genomic analysis of T. equi was undertaken to: 1) identify genes contributing to immune evasion and persistence in equid hosts, 2) identify genes involved in PBMC infection biology and 3) define the phylogenetic position of T. equi relative to sequenced apicomplexan parasites. (
  • TNF/iNOS-producing dendritic cells mediate innate immune defense against bacterial infection. (
  • Firstly, we analyzed the parasitical characteristics of the infection using inbred and outbred mouse strains to compare the impact of host genetic background on the infection and on survival rates. (
  • This success critically depends on the ability of parasites to activate a strong adaptive immune response during acute infection with tachyzoites that eliminates most of the parasites and to undergo stage conversion to bradyzoites that encyst and persist predominantly in the brain. (
  • SRS9 c but not wild-type parasites elicited a SRS9-specific immune response marked by IFN-γ production, suggesting that stage-specificity of SRS Ags determines their immunogenicity in infection. (
  • This acute infection with TZs activates strong, long-lasting Ab and T cell responses that eliminate most of the parasites ( 3 ). (
  • BZs then encyst, establish a chronic infection primarily in the brain and harmlessly persist for the life of an immunocompetent host. (
  • A key feature of Toxoplasma persistence is the requirement of a functional immune system to control the acute infection with TZs. (
  • In an immunodeficient host, uncontrolled TZ growth causes tissue destruction, and persistent infection is not established ( 5 ). (
  • An Interesting chapter deals with new insights into immune diagnosis in Trypanosoma cruzi infection, while another chapter on malaria vaccines critically reviews their development since the beginning, examining the basis for failures or successes encountered in clinical trials. (
  • During the first 4 days of infection, when parasite growth was limited, the coat served as a disposable, renewable barrier between parasite and host that was intermittently shed to cleanse the nematode of adhering host immune products. (
  • In the later infection phase the parasite grew rapidly and was beyond the effect of the depleted host immune response. (
  • In summary, shedding of the surface coat is an adaptive counter response by R. culicivorax to the mosquito immune reaction to infection and provides a classic example of host-parasite coevolution. (
  • This has left researchers unable to empirically distinguish/identify adaptive physiological changes enforced by the parasites from pathological side effects of infection, resulting in scientists relying on narratives to explain results, rather than empirical evidence. (
  • As with a majority of host manipulation research, the three cases presented above cannot categorically connect parasite establishment ( Event A ) with the physiological/molecular changes seen in infected hosts ( Event B ). Instead, one must correlate parasite presence with the observed physiological changes that coincide temporally with one or another stage of infection. (
  • In humans and veterinary hosts, T. gondii is frequently associated with congenital infection and abortion. (
  • This parasite can be transmitted by the vertical transmission of the rapidly growing tachyzoite form if an immunologically naïve mother acquires a new infection during pregnancy. (
  • In addition, T. gondii is an opportunistic pathogen associated with encephalitis or systemic infections in immunocompromised hosts such as individuals with advanced human immunodeficiency virus infection (i.e. (
  • Tachyzoites divide rapidly within host cells and are thought to be responsible for the clinical manifestations of infection. (
  • The reason I say this is "presumably" a immune evasion molecule is that the other possibility is that the response is driven by the host - that this is more analogous to the way rodents develop a regulatory T cell response to persistent viruses, reducing harmful inflammatory diseases but allowing long-term infection with the virus. (
  • 3) In humans and other intermediate hosts, Toxoplasma develops into a chronic infection that cannot be eliminated by the host's immune response or by currently used drugs. (
  • Both infection routes result in the infection of intestinal cells after which the parasites develop into tachyzoites, which are the fast-growing, disseminating form of the parasite. (
  • During the vertebrate infective stages, these parasites alter the differential expression of virulence genes, modifying their biological and antigenic properties in order to subvert the host protective immune responses and establish a persistent infection. (
  • During T. spiralis infection, Ts Pmy plays an important role in modulating the host immune system by stimulating DCs to differentiate the CD4 + T cells to regulatory T cells, in addition to binding to components of the host complement cascade, as survival strategies to live in host. (
  • During T. spiralis infection, the entire life-cycle is completed within the same host. (
  • How the Trichinella parasite maintains the chronic infection within the host without being recognized and attacked by the host's immune system remains unknown [ 4 ]. (
  • Understanding the mechanism underlying the immune evasion would greatly benefit the design of preventive/therapeutic vaccines or drugs to control the infection. (
  • Under normal circumstances, this would ensure quick recognition and clearance of the parasite, but T. brucei has evolved a mechanism for antigenic variation during infection in which the parasite can turn on and off VSG-encoding genes from a genomic repertoire of ~2000 different genes. (
  • 2015) has shown, however, that T. brucei parasites express a huge diversity of VSGs at any given time during an infection. (
  • Understand the broader consequences of parasite infection at both the individual host and host population level. (
  • Where Toxoplasma is unique, is that the parasite has little species restriction for a productive infection in the next host. (
  • Chronic infection in rodents make them less afraid of cat odor, thus facilitating being preyed upon by the definitive feline host. (
  • The Ibizian hound presents a predominantly cellular immune response against natural Leishmania infection. (
  • Infection of a vertebrate host is initiated by inoculation of sporozoite stage parasites into the bloodstream during the taking of a bloodmeal. (
  • During the acute babesial infection, the host may become severely ill. (
  • 1 ], who passively protected heifers against experimental intravaginal infection with C. fetus by systemic administration of immune serum. (
  • This partial immune protection was seen as evidence that enhancement of immunity may result in total clearance of infection. (
  • The level of internalization of parasites treated with the anti-115-kDa antibody into host macrophages was significantly reduced from that of non-antibody-treated parasites, suggesting that this serine protease probably plays a role in the infection process. (
  • Aside from its classic role in carbohydrate metabolism, enolase was recently found to localize to membranes, where it binds host plasminogen and functions as a virulence factor for several pathogens. (
  • Researchers in CSI-Dublin focus on frontier areas of innate immune sensing, immunometabolism, inflammatory T cell subsets and their regulation, evasion of immunity by pathogens, infectious disease and cancer vaccines and the genetic basis of immune- mediated diseases, such as inflammatory bowel disease. (
  • IRG activation in most cases is induced by an immune response and leads to clearance of certain pathogens. (
  • They are involved in important immune defenses against intracellular pathogens and as a result have become a target for immune evasion by those pathogens. (
  • IRGs Have Evolved From Invertebrates Studies to determine the evolutionary origins of vertebrates have led to understanding the development of immune system processes and furthermore answer the questions of how and why pathogens have learned to evade and shut down these selectable genetic traits. (
  • The groups in this research theme work on a wide variety of pathogens (protozoal and helminth parasites, fungi, bacteria and viruses) and hosts (mammals, fish, insects, nematodes and plants). (
  • While therapeutic strategies focusing on inhibiting inorganic sulfate assimilation and cysteine synthesis show promise in vitro, in vivo efficacy maybe limited due to the diversity of host-derived sulfur sources and the fact that most pathogens are capable of acquiring multiple sources of sulfur. (
  • Coevolution between hosts and pathogens is thought to occur between interacting molecules of both species. (
  • The coevolutionary arms race between hosts and pathogens is often described as a recurrent struggle for increased resistance in hosts and evasion of recognition by pathogens [1] - [3] . (
  • TIGR researchers are now tackling the genomes of the second major human malaria parasite, P. vivax, as well as deciphering the genetic codes of other pathogens that sicken or kill millions of people - including parasites that cause African sleeping sickness, Chagas disease, schistosomiasis, amoebic dysentery, lymphatic filariasis, and opportunistic infections in HIV/AIDS patients. (
  • Several pathogens of humans and domestic animals depend on hematophagous arthropods to transmit them from one vertebrate reservoir host to another and maintain them in an environment. (
  • Some pathogens are difficult to eradicate and require a potent immune response involving destructive and cytotoxic mediators, which can result in adverse effects and immunopathology. (
  • Mononuclear phagocytes can be used by intracellular pathogens to disseminate throughout the host. (
  • Parasites are one of these pathogens. (
  • Parasites of the genus Leishmania are able to secure their survival and propagation within their host by altering key signalling pathways involved in the ability of macrophages to directly kill pathogens or to activate cells of the adaptive immune system. (
  • The research in the last decade provided evidences of oxygen sensing mammalian transcription factor hypoxia-inducible factor-1 (HIF-1) as a master controller of innate immune response of phagocytes against various intracellular and extracellular pathogens. (
  • In response to most of these pathogens host phagocytes increase transcription of HIF-1α, the regulatory component of HIF-1, to express various effector molecules against invaders. (
  • Here, we review recent advances that illustrate how these virulence factors disarm innate immunity and promote survival of the parasite. (
  • Immunity Related Guanosine Triphosphatases or IRGs are proteins activated as part of an early immune response. (
  • The role of host eicosanoids in modulating immunity is well documented. (
  • The study, "Metabolome modulation of the host adaptive immunity in human malaria," published in the journal Nature Metabolism , provides insight into an area of research previously limited outside of the laboratory setting. (
  • Metabolome modulation of the host adaptive immunity in human malaria, Nature Metabolism (2021). (
  • After many years of exposure, individuals living in endemic areas develop a form of clinical immunity to disease known as premunition, which is characterised by low parasite burdens rather than sterilising immunity. (
  • The reason why malaria parasites persist under a state of premunition is unknown but it has been suggested that suppression of protective immunity might be a mechanism leading to parasite persistence. (
  • Since sheep develop acquired immunity against T. circumcincta , there is some potential for the development of a vaccine against this parasite. (
  • Dendritic cells (DCs) are antigen presenting cells that play a pivotal role in the control and modulation of immune responses by initiating T cell responses and producing cytokines and other molecules that regulate adaptive immunity [ 21 ]. (
  • and for the past few years I have been developing anti-filarial vaccines that target parasite immune modulators and thus limit the ability of these worms to evade host immune responses. (
  • Immune responses to macroparasites are sensitive to the interaction between genetic growth potential and protein nutrition in mice. (
  • Originally developed for protection against host immune responses, viral immune-modulating proteins are extraordinarily potent, often functioning at picomolar concentrations. (
  • Innate and adaptive responses are tightly controlled by anti-inflammatory cytokines and regulatory T cells and a failure in immune regulation can result in inflammation and immune responses to self-antigens and the development of autoimmune and other immune-mediated diseases. (
  • and (3) inhibiting immune responses by favoring immune cell apoptosis. (
  • 2) inducing immune responses such as those related to the function of monocyte-macrophages, NK cells, T cells, and B cells. (
  • Eicosanoids are a subset of oxylipins and include the prostaglandins and leukotrienes, which are potent regulators of host immune responses. (
  • The precise role of pathogen-derived eicosanoids in pathogenesis remains to be determined, but the potential link between pathogen eicosanoids and the development of TH2 responses in the host is intriguing. (
  • Mammalian prostaglandins and leukotrienes have been studied extensively, and these molecules can modulate Th1 versus Th2 immune responses, chemokine production, phagocytosis, lymphocyte proliferation, and leukocyte chemotaxis. (
  • These eicosanoids are potent modulators of immune responses in addition to playing a role in numerous basic host physiologic processes ( 40 ). (
  • Antiviral responses also occur in the nucleus, yet these intranuclear innate immune responses are poorly defined at the receptor-proximal level. (
  • Specific topics covered within the course will include: parasite biochemistry, ecology, parasite evasion of the host immune system, host immune responses, and host behavior. (
  • Guardee evolution may be governed by a counterbalance between improved activation in the presence and prevention of auto-immune responses in the absence of the corresponding pathogen. (
  • In a sort of complex disguise, the parasite evades the host's immune response by expressing different versions of the proteins on the blood cell's surface - thus confounding the immune responses that aim to destroy the infected cells. (
  • These antigens can vary from strain to strain to the extent that the strain-specific immune responses of vertebrate reservoirs determine the population structure of the pathogen. (
  • OspC sequences are diverse, and the immune responses to them appear to provide for balancing selection. (
  • Lymphoid populations exerting immunosuppressive activity, such as natural regulatory T (T reg ) cells, have been shown to play a critical role in balancing protective immune responses and immune-mediated pathology [1] - [4] . (
  • Many parasites induce the secretion of molecules that influence the physiological and immunological responses in hosts, including intermediaries and vectors. (
  • Conversely, parasites themselves are phylogenetically diverse, target a range of different tissues, and have evolved numerous alternative strategies to evade or inhibit protective immune responses by strategies, such as antigenic variation, molecular mimicry or affecting antigen processing and presentation. (
  • Osaka, Japan - The current COVID-19 climate has made vaccines, antibodies, and immune responses topics of everyday conversation. (
  • Like most biological processes, immune responses are complicated. (
  • Humoral and Cellular Immune Responses to Glucose Regulated Protein 78 -- a Novel Leishmania Donovani Antigen Tropical Medicine & International Health : TM & IH. (
  • The treatment of the disease is severely underdeveloped due to the ability of the Leishmania pathogen to evade and abate immune responses. (
  • Host CD4+ and CD8+ responses can then be induced following intracellular synthesis, processing and HLA (Human Leukocyte Antigen) presentation of class I and II T-cell epitopes. (
  • Another immune-evasion mechanism commonly used in microbial persistence is the variation of antigenic composition that eliminates epitopes that would otherwise be targeted by protective immune responses ( 12 , 13 , 14 ). (
  • For ES proteins, key pathways, including Fc epsilon RI, T cell receptor, and chemokine signalling as well as leukocyte transendothelial migration were inferred to be linked to immune responses, along with other pathways related to neurodegenerative diseases and infectious diseases, which warrant detailed future studies. (
  • It's long been known that parasitic worms - now rare in the West, but until recently a normal part of the human condition - induce an immune response that is broadly similar to a lot of allergic responses. (
  • Cellular and humoral immune responses in dogs experimentally and naturally infected with Leishmania infantum. (
  • Proteases are a ubiquitous group of enzymes that play key roles in the life cycle of parasites, in the host-parasite relationship, and in the pathogenesis of parasitic diseases. (
  • This paper is dedicated to discussions of the pathogenesis and the means for evasion used by viruses in their battle with the immune system. (
  • A. A. Rascon and J. H. McKerrow, "Synthetic and Natural Protease Inhibitors Provide Insights into Parasite Development, Virulence and Pathogenesis", Current Medicinal Chemistry (2013) 20: 3078. (
  • Describe The Modes Of Transmission, Pathogenesis And Host-Pathogen Interaction Of Medically Important Microorganisms And Outline The Basic Concepts Of Laboratory Diagnosis, Prevention And Treatment Of Infectious Diseases. (
  • The aim of the current study was to evaluate the effects and putative mechanism of action of evasin-1, a novel CCL3-binding protein, in the pathogenesis of acute graft-versus-host disease (GVHD). (
  • These findings help us understand the immune biology of capsular polysaccharides in fungal pathogenesis. (
  • However, few studies have addressed serine proteases in Leishmania and their role in host pathogenesis. (
  • Recent advances in genomic analysis of several of the major global parasites have revealed key factors involved in the pathogenesis of parasite diseases. (
  • These drugs showed the ability to inhibit cruzipain, by diminishing the burden of the parasite in skeletal and cardiac muscles, as well as by reducing the inflammatory response in the tissues of Trypanosoma cruzi infected mice. (
  • Trypanosoma cruzi have a large repertoire of genes (and pseudogenes) encoding mucin and mucin-associated surface proteins (MASPs), which are heterogeneously expressed in parasite populations. (
  • Several different species may cause animal trypanosomosis and although Trypanosoma vivax (sub-genus Duttonella ) is currently responsible for the vast majority of debilitating cases causing great economic hardship in West Africa and South America, little is known about its biology and interaction with its hosts. (
  • Chagas disease (CD) is a neglected disease caused by the parasite Trypanosoma cruzi , which affects underdeveloped countries. (
  • Parasites are organisms found in almost every niche and some species have evolved to the point of developing characteristics for intracellular survival, which is the case of the parasite Trypanosoma cruzi that causes Chagas disease. (
  • Glycolysis is essential to Trypanosoma brucei (Tb), the protozoan parasite that causes African sleeping sickness in humans and nagana in livestock, and to Trypanosoma cruzi (Tc), that causes Chagas ' Disease. (
  • Trypanosoma vivax is one of the most common parasites responsible for animal trypanosomosis, and although this disease is widespread in Africa and Latin America, very few studies have been conducted on the parasite's biology. (
  • Trypanosoma vivax is a major parasite of domestic animals in Africa and Americas. (
  • Trypanosoma vivax and Trypanosoma congolense are the main parasite species responsible for Animal African Trypanosomosis (AAT) or Nagana . (
  • Written by a team of authors active in the field of Leishmania and Trypanosoma research, this volume reviews the current research in kinetoplastid parasites. (
  • Trypanosoma cruzi is an obligatory intracellular protozoan parasite, and it is the etiological agent of Chagas' disease that is endemic in the Americas. (
  • The causative agent of both human and animal trypanosomiasis is Trypanosoma brucei, a protozoan parasite covered by a dense variant surface glycoprotein (VSG) coat. (
  • In the parasite Trypanosoma brucei , which is distantly related to the better characterised animals and fungi, exceptionally fast endocytic turnover aids its evasion of the host immune system. (
  • The oligopeptidase B of Leishmania regulates parasite enolase and immune evasion. (
  • Protozoan parasites like Leishmania predominantly express Clan CA cysteine proteases for key life cycle functions. (
  • Insect vector stages of the parasites ( Leishmania promastigotes and T. cruzi epimastigotes, white bar ) were compared with the vertebrate host stages (amastigotes, black bar ) for L. donovani , L. mexicana , and T. cruzi . (
  • T. brucei and related parasites ( T. cruzi and Leishmania ) undergo many developmental changes as they alternate between a mammalian host and the insect vector. (
  • In this chapter, we address the relationship between Leishmania and its host macrophage at the molecular level. (
  • One important step in this immune evasion process is the Leishmania-induced activation of host protein tyrosine phosphatase SHP-1. (
  • The most important Leishmania parasite that infects domestic animals is L. infantum , also known as L. chagasi in Latin America. (
  • Development of a reverse transcriptase loop-mediated isothermal amplification (LAMP) assay for the sensitive detection of Leishmania parasites in clinical samples. (
  • Lundep, a sand fly salivary endonuclease increases leishmania parasite survival in neutrophils and inhibits XIIa contact activation in human plasma. (
  • Leishmania , a protozoan parasite, constitutes a major source of human mortality and morbidity. (
  • However, more recent evidences revealed that protozoan parasite Leishmania donovani (LD), the causative agent of fatal visceral leishmaniasis, in contrary could promote and exploit HIF-1 activation for its survival advantage within host macrophages. (
  • This study demonstrates that in addition to an increase in Leishmania -specific humoral immune response in Ibizian hounds, a parallel increase in cellular immune response was observed. (
  • Leishmania species have a relatively simple life cycle, with parasite stage differentiation regulated by environmental signals encountered in their different hosts. (
  • Despite this, the use of virus-derived proteins as natural sources for immune modulators remains in the early stages of development. (
  • These proteins provide a new and natural source for immune-modulating therapeutics, similar in many ways to penicillin being developed from mold or streptokinase from bacteria. (
  • In particular, human complement regulators are co-opted by parasite adhesins and surface proteins for parasite invasion and to evade complement attack. (
  • iSP-RAAC: Identify secretory proteins of malaria parasite using reduced amino acid composition. (
  • These genes contain hypervariable regions and produce highly O-glycosylated proteins that are potentially involved in host immune evasion and host cell interaction. (
  • The virulence of this parasite is reliant upon the mutually exclusive expression of cytoadherence proteins encoded by the 60-member var gene family. (
  • Helminths (worms) depend on several classes of proteases for development, host tissue invasion and migration, and for degradation of host hemoglobin and serum proteins. (
  • According to the "Guard-Hypothesis," R proteins (the "guards") can sense modification of target molecules in the host (the "guardees") by pathogen effectors and subsequently trigger the defense response. (
  • Gardner said the genome analysis identified about 200 parasite genes that produce proteins involved in that elaborate evasion. (
  • Previous research had shown that, during the stage of its life cycle when it develops inside red blood cells, the parasite produces at least two types of proteins that are exposed on the surface of the infected blood cells. (
  • That location makes it easier for the parasite - during the reproductive stage when it is carried by a mosquito - to alter the structure of these proteins through changes in the genes that encode them. (
  • Gardner said the genome sequence now defines, for the first time, a complete set of those evasive proteins from a single parasite. (
  • The PfEMP1 are among the few parasite proteins constantly exposed to the host immune system during the blood phase of the parasite life cycle. (
  • Binding of infected red blood cells to blood vessels is mediated by a large and diverse family of parasite adhesion proteins, called PfEMP1. (
  • As the parasite switches between different PfEMP1 proteins, this determines parasite-binding tropism for different blood vessels. (
  • We recently identified a distinct subset of PfEMP1 proteins that binds to brain endothelial cells using a host receptor called endothelial protein C receptor (EPCR). (
  • Since excellent reviews were produced in the last decade regarding the roles played by proteases in the vertebrate hosts, we focused in the recent developments in our understanding of the biochemistry and cell biology of gp63-like proteins in lower trypanosomatids. (
  • This is presumably a parasite immune evasion molecule, analogous in concept to the many viral proteins that block TLR pathways. (
  • These proteins also undergo clonal antigenic variation as a means of immune evasion. (
  • the proteases are involved in the invasion of the host via parasite migration through tissue barriers, degradation of host proteins for their nutrition, immune evasion, and activation of inflammation ( 21 ). (
  • Antigenic variation is the means by which a number of highly pathogenic microorganisms, ranging from the electronmicroscopic human viruses to bacteria to fungi and unicellular protozoan parasites, passively evade immune surveillance. (
  • Macrophage-mediated innate host defense against protozoan parasites. (
  • are kinetoplastid protozoan parasites that infect numerous mammalian hosts, including humans, and are transmitted by the bite of female phlebotomine sand flies. (
  • Kinetoplastida trypanosomatidae microorganisms are protozoan parasites exhibiting a developmental stage in the gut of insect vectors and tissues of vertebrate hosts. (
  • True antigenic variation, however, arises in a single clone or genotype in a single host and "involves the loss, gain, or change in a particular antigenic group, usually by loss, gain, or change in one of the polypeptide or polysaccharide antigens…" (3) . (
  • Viruses are also said to have antigenic variation but are excluded from this review because the mechanism they use usually depends either on the accumulation of point mutations in a single genotype (e.g., the antigenic drift of influenza A virus) or on recombination or reassortment between two different genotypes infecting the same host (e.g., antigenic shift of influenza A virus). (
  • Antigenic variation is a major mechanism of passively evading the host immune surveillance. (
  • To avoid immune destruction, malaria parasites use a clever strategy called clonal antigenic variation to control PfEMP1 expression and specifically express only one PfEMP1 on the red blood cell membrane at a time. (
  • Parasites have evolved a range of evasion strategies, including absorption of host antigen, antigenic variation, immuno-suppression and use of immunologically privileged sites. (
  • What role do extravascular parasites play in antigenic variation and immune evasion? (
  • The first evidence for antigenic variation in babesial parasites was obtained with Babesia rodhaini [22] and later with B. bovis [23]. (
  • Cruzipain aids in the process of breaking down host tissue and is prepared to signal the escape mechanism if it detects any response from the host's immune system. (
  • In other cases, effects are mediated indirectly via the host's immune system. (
  • A team of developmental biologists at the Morgridge Institute for Research has discovered a means by which schistosomes, parasitic worms that infect more than 200 million people in tropical climates, are able to outfox the host's immune system. (
  • To cope with these constant threats, the host's immune system has evolved to become one of the most complex organs known. (
  • Occasionally, cysts reactivate and growth of newly emerged parasites must be controlled by the host's immune system or disease will occur. (
  • Immunological modulation and evasion by helminth parasites in human populations. (
  • Helminth parasites are highly prevalent in human communities in developing countries. (
  • G. Escobedo, L. Lopez-Griego, and J. Morales-Montor, "Neuroimmunoendocrine modulation in the host by helminth parasites: a novel form of host-parasite coevolution? (
  • Owing to the control of insect vector populations, the safe disposal of human excrement, and the availability of efficacious drugs, helminth parasites have been largely eradicated as a public health concern in developed countries. (
  • One consequence of this geopolitical segregation is that most of the world's pharmaceutical industries do not support active research and development programs on helminth parasites that cause human disease. (
  • Many helminth parasites are long-lived and cause chronic infections. (
  • Cowman AF, Berry D, Baum J (2012) The cellular and molecular basis for malaria parasite invasion of the human red blood cell. (
  • It combines classical descriptive biology of parasites with modern cell and molecular biology approaches, and also addresses parasite evolution and ecology. (
  • Parasites found in mammals, non-mammalian vertebrates, and invertebrates are systematically treated, incorporating the latest knowledge about their cell and molecular biology. (
  • Particular emphasis will be put on the molecular interplay between the host and parasite to understand how bacteria breach natural host barrier, how they exploit new niches in the host and avoid host defense mechanism. (
  • 3. Differentiate the progress of modern molecular biology technologies to increase understanding of the host-parasite relationships, improve parasite diagnosis and support anti-parasite therapy discovery. (
  • disease can be diagnosed by microscopy, isolation of the parasite, serology or other molecular techniques. (
  • Several serological and molecular diagnostic methods have been developed, but the gold standard is still the demonstration of parasites in stained tissue smears. (
  • Improved insights into the molecular biology of this parasite could underpin alternative methods required to control this and related parasites, in order to circumvent major problems associated with anthelmintic resistance. (
  • The results provide a comprehensive insight into the molecular biology of this parasite and disease manifestation which provides potential focal point for future research. (
  • However, the molecular evidence for adaptive behavioural manipulation (behavioural change in the host that directly benefits the parasite) in a majority of host-parasite associations is missing crucial pieces of evidence. (
  • Here, we describe a draft genome and developmentally staged transcriptome of H. contortus to substantially improve our understanding of this parasite at the molecular level. (
  • Emphasis will be on the major parasites that cause human and animal disease covering molecular, cellular, in vitro and in vivo experimental approaches for the study of host parasite relationships. (
  • Four protein species were significantly elevated in OPB(-/-) parasites, and all four were identified by mass spectrometry as enolase. (
  • The variations between and within species suggest a high rate of evolutionary change for this particular element of host pathogen interaction and highlight the importance of understanding the limitations of using model systems to study human immunology. (
  • Rabies and yellow fever viruses have reservoirs in alternative animal hosts, such as in feral species. (
  • We discuss here the specific host processes that have been shown to restrict bacterial presence in the glands and crypts, specifically the immune system, acid, mucin, oxygen, and reactive oxygen species. (
  • Species belonging to both phyla occupy numerous niches within their mammalian hosts, ranging from intestinal lumen to intravascular and even intracellular sites. (
  • The species shown here, Schistosoma mansoni, lives inside host blood vessels, where it takes up nutrients that fuel its growth and reproduction. (
  • The parasites hatch from eggs released via human waste and infect a specific species of snail. (
  • There are multiple species of parasites that are known today and each one is unique. (
  • The observation that certain species of parasite may adaptively manipulate its host behaviour is a fascinating phenomenon. (
  • Integrate data and information gained from different parasite species and from different experimental approaches to gain a clear overview of our current knowledge of parasitic disease and the major challenges that remain. (
  • While a zoonosis in humans, this simian malaria parasite species infects macaque monkeys and serves as an experimental model for in vivo, ex vivo and in vitro studies. (
  • Lack of effective vaccines and emergence of drug-resistant parasites and insecticide-resistant mosquito vectors are the main reasons for the failure in controlling the parasites and the associated disease. (
  • Life cycles, development and modes of transmission will include accounts of the importance of direct transmission, the role of vectors and intermediate hosts, zoonoses and reproductive potential (Ro). (
  • In addition, we describe the development of appropriate vectors for parasite transgenesis and selection in vitro and their use in analyzing genetically modified parasite lines. (
  • They are digenetic parasites: the flagellated promastigote forms, which can be derived in axenic culture, differentiate within the alimentary tracts of sandfly vectors from a replicating procyclic to a nonreplicating, infectious metacyclic stage, whereas obligately intracellular amastigotes live and replicate in mammalian mononuclear phagocytes, such as macrophages ( 1 ). (
  • Toxoplasma gondii is a common parasite of animals and humans and can cause serious opportunistic infections. (
  • Toxoplasma gondii , once an obscure protozoan parasite, has recently become the focus of intense research, both as a serious pathogen in its own right and as a model member of the phylum Apicomplexa. (
  • The intracellular protozoan parasite Toxoplasma gondii has been shown to target IRGs in mice allowing for resistance from the host immune response. (
  • Toxoplasma gondii is an obligate intracellular parasite that is prevalent worldwide. (
  • Toxoplasma persists in the face of a functional immune system. (
  • Toxoplasma gondii is an obligate intracellular, protozoan parasite highly prevalent in warm-blooded vertebrates ( 1 ). (
  • Another characteristic of Toxoplasma persistence is that the parasite persists in the face of a long-lasting anti- Toxoplasma immune response. (
  • Toxoplasma succeeds in this daunting task by using a variety of strategies applied by microbial agents, which allow them to persist until transmission to a new host (by carnivorism for Toxoplasma ) can be accomplished. (
  • Toxoplasma gondii , an apicomplexan parasite of mammals, was first identified over 100 years ago (in 1908) by Nicolle and Manceaux, who isolated tachyzoites from the gundi, a North African rodent ( 34 ). (
  • Ocular toxoplasmosis, which is caused by the protozoan parasite Toxoplasma gondii , is the leading cause of retinochoroiditis. (
  • Toxoplasma gondii is an obligate intracellular Apicomplexan parasite that can infect a wide range of warm-blooded animals including humans [ 1 ]. (
  • 2) Toxoplasma has an extremely wide host cell tropism that includes most nucleated cells. (
  • Toxoplasma strains differ in how they manipulate immune signaling pathways. (
  • Toxoplasma gondii is considered by and large the most successful parasite of warm blooded animals. (
  • Toxoplasma is an orally acquired parasite that enters the body through the small intestine and disseminates to the brain, heart and muscle tissues. (
  • At these sites Toxoplasma becomes dormant and forms a cyst wall around itself protecting the parasite against the attacks of the immune system and anti-parasitic drugs. (
  • Toxoplasma has therefore mastered the art of stealth and immune evasion. (
  • Toxoplasma's broad host range and massive amplification during its sexual cycle contributes to the global prevalence and survival of Toxoplasma . (
  • Toxoplasma can also spread between intermediate hosts through carnivorous activity. (
  • Babayan S. A. , Luo H. L., Gray N., Taylor D. W., Allen J. E. (2012) Deletion of parasite immune modulatory sequences combined with immune activating signals enhances vaccine mediated protection against filarial nematodes. (
  • surface of the parasite and their functional importance, many show promise as vaccine candidates. (
  • We have solved the structure of the immunologically important portion of the vaccine candidate MSP-1, a GPI linked protein expressed on the surface of the merozoite form of the parasite. (
  • One of the challenges for malaria vaccine development is the complex life cycle and high polymorphism of P. falciparum parasite strains in the parasite population. (
  • The Smith Lab is interested in vaccine approaches to inhibit parasite invasion into host cells or prevent cytoadhesion of infected erythrocytes. (
  • As malaria is an intracellular parasite, it is likely that a protective vaccine would activate the cellular arm of the immune response and be effective against the pre-erythrocytic liver stage of the life cycle. (
  • Apoptosis and its Impact on the Parasite-Host Interaction 9. (
  • These details are determinant in the equilibrium of the pathogen-host interaction and the result of this relation, which can vary from symbiosis, mutualism or parasitism. (
  • There is a complex interaction between parasites and the immune systems of their hosts. (
  • The relationships between parasites and hosts are complex and there is substantial interaction, communication and biochemical co-evolution. (
  • Studies on its biology, metabolism and interaction with the host immune system have been hindered by a lack of suitable tools for its maintenance in vitro and its genetic engineering. (
  • First described in 1901 as Piroplasma equi, this re-emergent apicomplexan parasite was renamed Babesia equi and subsequently Theileria equi, reflecting an uncertain taxonomy. (
  • are a diverse group of tick-borne, obligate, intraerythrocytic Apicomplexan parasites infecting a wide variety of organisms. (
  • Kinetoplastid parasites are responsible for a number of serious protozoal diseases with limited treatment options and few commercially available vaccines. (
  • Although vaccines using some native parasite antigens (called H11 or H-gal-GP) can partially prevent haemonchosis in experimental sheep, homologous recombinant molecules have failed to achieve protection [ 6 ]. (
  • Describe the current challenges of parasite control and the progress of anti-parasitic vaccines. (
  • As a requirement for invasion into the red cell of a mammalian host, MSP-1 undergoes two proteolytic processing stages. (
  • Usually, the life stage responsible for infecting the mammalian host is the larva, and the larva must migrate within the host to its appropriate niche where it can grow and reproduce. (
  • when the metacyclic promastigote is inside the mammalian host. (
  • Stem cells in the parasite are necessary for their survival and reproduction, but their role during the early stages inside the mammalian host has been unclear. (
  • However, since current culture conditions do not fully reflect the in vivo environment of the host vasculature (such as the lack of host immune cells and blood flow), the team decided to take the project further by examining the function of the gland when the parasite is living inside the mammalian host. (
  • The work presented herein focused on determining axenic conditions for culturing and growing insect (epimastigote) forms of T. vivax and prompting their differentiation into metacyclic forms that are infectious for the mammalian host. (
  • Most parasites rely on their intracellular and extracellular protease repertoire to invade and multiply in mammalian host cells. (
  • PfEMP1] appears to play a central role in the adhesion of parasitised RBCs to specific receptors in the host micro-vasculature, and is thus critically important for the survival of the parasites because it prevents destruction of the infected RBCs during their passage through the spleen. (
  • The structure of parasites will be described in relation to the insight these studies provide into parasite survival both within the host and during the free-living stages. (
  • Morgridge postdoctoral fellow Jayhun Lee and colleagues reported in today's issue of Proceedings of the National Academy of Sciences (PNAS) that the parasite's esophageal gland , an accessory organ of the digestive tract, mediates an immune-evasion mechanism that is essential for survival in the host . (
  • Suspecting that the esophageal gland might be important for the survival of the parasites, the team disrupted a gene critical for making the esophageal gland and cultured the parasites in a dish. (
  • This chapter is based on the metabolic differences between the pathogenic parasite and mammal hosts that led to the progress in the search for novel metabolic pathways in parasites that may be essential for parasite's survival but with no counterpart in the host. (
  • Intracellular parasites use host components for their survival and growth after invasion within host, while hosts spread out their innate immune defences to deny any advantage to the invading parasite. (
  • Babesial parasites clearly have adapted well to survival in the hostile environment that is the immune host. (
  • The other is hit and stay with viral persistence in the same host. (
  • To test the contribution of this antigenic switch to parasite persistence, we engineered parasites to constitutively express the normally bradyzoite-specific SRS9 (SRS9 c ) mutants and tachyzoite-specific SAG1 (SAG1 c ) mutants. (
  • These findings strongly suggest that B-1 cells and B-1CDP cells have a potential role in the persistence of the parasite in host cells. (
  • Parasites and infectious diseases are everywhere and represent some of the most potent forces shaping the natural world. (
  • For infectious agents, the means for host recovery is one of detection, apprehension, and destruction of the parasite by the immune system. (
  • Parasites comprise a group of organisms that cause a massive infectious disease problem for humans and several animals of veterinary importance. (
  • Bradyzoite conversion is a critical step in the parasite's life cycle since bradyzoites are impervious to immune-mediated destruction, are relatively non-immunogenic, and are the infectious form of the parasite during horizontal transmission (e.g. digestion of undercooked meat). (
  • This protective structure, called the tissue cyst , is infectious and allows the parasite to survive the digestive environment of the next host should it be consumed unsuspectingly by another hungry animal. (
  • Not diagrammed: Oocysts are also infectious to cats and vertical transmission in intermediate hosts. (
  • Our method for accurate mSFP detection and the mSFP identified will greatly facilitate large-scale studies of genome variation in the P. falciparum parasite and provide useful resources for mapping important parasite traits. (
  • We established a set of SFP calling parameters that could predict mSFP (SFP called by multiple overlapping probes) with high accuracy (≥ 94%) and identified 121,087 mSFP genome-wide from five parasite isolates including 40,354 unique mSFP (excluding those from multi-gene families) and ~18,000 new mSFP, producing a genetic map with an average of one unique mSFP per 570 bp. (
  • Genetic variation in parasites can contribute to drug resistance, immune evasion, and disease manifestation. (
  • This results in the maintenance of genetic diversity at pathogen antigens (or so-called effectors) and host resistance genes such as the major histocompatibility complex (MHC) in mammals or resistance ( R ) genes in plants. (
  • Rockville, MD - In a landmark contribution to the age-old battle against malaria, a consortium of scientists including The Institute for Genomic Research (TIGR) announced today that they have deciphered the complex genetic code of the parasite that causes the deadliest form of the disease. (
  • She added: "The lessons we learned from the work on the malaria parasite's genetic code are now helping TIGR and others to investigate a host of other parasites. (
  • These approaches should bring us the means to track genetic variation of parasites and drug resistance, integrating this knowledge into effective stewardship programs to prevent vector-borne kinetoplastid infections in areas at risk of disease spreading. (
  • Members of the cat family ( Felidae ) are the only known definitive host, meaning this is where the parasite undergoes genetic recombination and sexual reproduction. (
  • Genetic and genomic approaches for the discovery of parasite genes involved in antimalarial drug resistance. (
  • Written by internationally acclaimed researchers, this is the first book to provide a comprehensive coverage of this important parasite from both the host and pathogen perspectives. (
  • Sulfur is a requirement for bacterial growth and inorganic and organic sulfur-containing metabolites are abundant within the host-pathogen interface. (
  • The malaria parasite's success as a pathogen depends partly on its ability to evade elimination by the human immune system. (
  • Without access to another vertebrate host through an arthropod, the pathogen will die with the host. (
  • Currently, the horse parasite Theileria equi is a re-emergent pathogen in parts of the United States after many years' absence. (
  • Further attachment of the glycodendrimer to a biocompatible, surface eroding microparticle allows for targeted uptake and internalization of the pathogen-associated oligosaccharide by phagocytic immune cells. (
  • It is possible that IRGs may have existed prior to the Cambrian Explosion as an innate immune mechanism and with the evolution of the adaptive immune system in vertebrates, IFN evolved to modulate IRG function. (
  • The unit provides an in-depth covering of contemporary parasitology concentrating on the complex relationship between parasite and host. (
  • The aim of the unit is to provide an in-depth understanding of contemporary parasitology concentrating on the complex relationship between parasite and host. (
  • One of the peculiarities of P. falciparum is that it is suggests this may be so, with implications for parasite drug-resistance studies[11]. (
  • Many of the parasitic worms have complex multistage life cycles that involve several hosts. (
  • The role of certain hormones in parasitic infections has been demonstrated, and there are documented direct effects of hormones on parasites. (
  • The host immune system rapidly recognised invading parasites, as granulocytes and discharged granules were observed attached to parasitic nematodes within 5 min. (
  • Melendez et al show that one class of parasitic worms make a protein that inhibits the anti-parasitic immune response. (
  • The strategies used by the hosts to control parasites and that the parasites use for immune evasion will form central themes together with an exploration of the consequences of parasitic disease for global health and current approaches of parasite control including vaccination. (
  • Parasites Kinetoplastids cause a number of serious diseases that have contributed to death and health problems in humans. (
  • Graft-versus-host disease (GVHD) is a major complication of allogeneic bone marrow transplantation (BMT), leading to significant morbidity and mortality in humans ( 1 ). (
  • In humans and other intermediate hosts, infections are the result of digesting parasites shed in felid feces or present in undercooked meat [ 4 ]. (
  • The strongylid nematode Haemonchus contortus (barber's pole worm) is one of the most important parasites of livestock, and represents a large order of nematodes (Strongylida) that infect both animals and humans worldwide [ 1 - 3 ]. (
  • T. gondii is unusual in that its propagation does not require passage through the definitive host (felids in whose intestinal tissues the sexual cycle occurs). (
  • During the first phase, the conditioning regimen (irradiation and/or chemotherapy) leads to damage, activation of host tissues, including intestinal mucosa, and induces the secretion of inflammatory cytokines ( 8 - 11 ). (
  • Parasites then disseminate to target tissues that include the retina where they then develop into long-lived asymptomatic tissue cysts. (
  • The migration of the parasite in host tissues is mediated by the release of proteolytic enzymes that can degrade the tissue barriers. (
  • Whereas wild type parasites elicited little, if any, response from infected macrophages, OPB(-/-) parasites induced a massive up-regulation in gene transcription. (
  • Filarial Parasites Develop Faster and Reproduce Earlier in Response to Host Immune Effectors Which Determine Filarial Life Expectancy. (
  • The unique nature of the Centre and the broader III research Theme represents a new frontier in the effort to understand and manipulate the many diseases where the immune response plays a central role in protection or pathology. (
  • Cruzipain is involved in aiding the parasite in penetrating and evading the immune response of the host. (
  • It is found to aid the parasite in entering the host cell and in evading an immune response. (
  • Cruzipain can help parasites escape the response from the adaptive immune system by interfering with the functions of immunoglobulins from the immunoglobin G subclasses. (
  • In response, parasites have again found ways to manipulate and exploit their hosts. (
  • Suppression of the Immune Response by a Soluble Complement Receptor of B Lymphocytes, 254:102-105 (1991). (
  • The adaptive immune system of an infected vertebrate selects against the original infecting serotype, but that specific response is ineffective against new variants. (
  • We restrict this review to situations in which an immune response against an antigen is synonymous with selection for another allele in the population. (
  • The immune response that develops during this time often proceeds to cause pathologic changes that in many helminth infections are the primary cause of disease. (
  • This immune evasion strategy enables parasites to gradually express different members of the PfEMP1 family and stay one step ahead of the host antibody response. (
  • This paradigm implies that the sexual dimorphism in response to parasites is mediated primarily by the immune system of the host, which disregards the ability of some parasites to directly respond to the distinct sex steroid hormone profiles of their female and male hosts [ 2 , 4 ]. (
  • Now, it isn't just immunologists who want to know how our bodies respond to re-infections months, years, or sometimes decades after an initial immune response. (
  • The induction of a SRS9-specific immune response correlated with a continual decrease in the number of SRS9 c cysts persisting in the brain. (
  • Some parasites that survive undergo stage conversion to BZs, a process that may be induced by the immune response itself ( 4 ). (
  • We identified a number of pathways responsible for immune response. (
  • Once parasite reach their target tissue they respond to the resulting IFNγ-based T h 1 response by transforming into bradyzoites. (
  • B-1 cells can directly and indirectly influence the immune response. (
  • Using the contrast between the resistant ITT and the highly susceptible Merino in a combined functional and comparative genomics approach, we have identified putative QTL (quantitative trait loci) for an extensive panel of parasite and immune response phenotypes and putative resistance pathways and effector molecules. (
  • Once erythrocyte invasion occurs, a seemingly perpetual cycle of asexual reproduction is established, despite the rapid development of a strong immune response [4]. (
  • The highly antigenic VSG is so densely packed on the parasite cell surface that it effectively obscures all other antigens from immune recognition. (
  • As the agents that cause bovine theileriosis infect and transform host cell PBMCs, we confirmed that T. equi infects equine PBMCs, however, there is no evidence of host cell transformation. (
  • The parasite can then infect these immune cells and use them to disseminate throughout their hosts [ 5 , 6 ]. (
  • T. cruzi is transmitted to the vertebrate host through the feces of triatomine bugs in which the infective forms, metacyclic trypomastigotes, are inoculated after the insect bite. (
  • However, these studies are also beginning to reveal the duality of the complement system in mediating both parasite destruction and facilitating efficient parasite invasion. (
  • Biryukov S, Angov E, Landmesser ME, Spring MD, Ockenhouse CF, Stoute JA (2016) Complement and antibody-mediated enhancement of red blood cell invasion and growth of malaria parasites. (
  • We have solved the structure of the two domains anchored to the parasite membrane at the end of the invasion process. (
  • Cysteine proteases in Entamoeba facilitate invasion of the host colon. (
  • hence, they are thought to play vital roles in the host tissue invasion process ( 17 ). (
  • Fundamental discoveries made by PIs (e.g. in the areas of innate immune receptors and signalling and Th17 cells) will be applied to disease via collaboration with clinicians and will be validated by the generation of probes and structures by chemists and Pharmacologists in TBSI. (
  • Among the major virulence factors identified are parasite-derived proteases. (
  • Currently, a community effort is underway to collect single nucleotide polymorphisms (SNP) from the parasite genome. (
  • We found that probe GC content, SNP position in a probe, probe coverage, and signal ratio cutoff values were important factors for accurate detection of SFP in the parasite genome. (
  • Further genome studies of other P. falciparum parasites isolated from malaria patients will identify other variants and provide insights into the pathogen's immune evasion process. (
  • The genome analysis revealed many of the parasite's metabolic pathways - the processes by which the parasite produces the energy and components it needs to survive. (
  • Indeed, a number of genes identified as potential manipulators of the host cell phenotype are absent from the T. equi genome. (
  • We provide a draft of the genome and the transcriptomes of all key developmental stages of H. contortus to support biological and biotechnological research areas of this and related parasites. (
  • This first draft genome of any strongylid nematode paves the way for a rapid acceleration in our understanding of a wide range of socioeconomically important parasites of one of the largest nematode orders. (
  • how does the immune system integrate the myriad sources of natural variation to maintain health? (
  • Immunology is the study of the immune system, which has evolved to protect the body against pathogenic viruses, bacteria and parasites and also functions in protection against cancer. (
  • These receptors function in cell adhesion, entry into host cells, and immune system evasion. (
  • However, most of what is known about eicosanoids stems from investigation of mammalian biology, most often in the context of immune system regulation. (
  • Persistent viral infections causing serious diseases derive, primarily, from altered function of the immune system. (
  • Viewed simply, the inappropriate or inadequate interface between host and invader or between host and its own immune system brings together an array of diseases of individual diversity that are the topics for this colloquium. (
  • This is complemented by work on the vertebrate immune system, with interests in haematopoiesis, NK cell development and function, inflammation and cytotoxicity. (
  • Then, when the host immune system eliminates the larger population, the minority population will take over, with another switch variant the immune system hasn't seen waiting in the wings. (
  • Describe The Main Constituents Of The Immune System, Their Development And Function. (
  • One big question we're interested in is how these parasites can thrive for decades in the bloodstream, while avoiding the host immune system ," says Lee. (
  • The broad host range of R. culcivorax within culicines may be partly a function of the nonspecific defence it mounts against the host immune system. (
  • Except for interfering with host complement system, whether Ts Pmy is involved in other immunomodulatory function is unknown. (
  • As the VSG expressed by a population of parasites is recognized by the immune system and then cleared, a minority of parasites will "switch" their VSG coat, turning on a new, and likely antigenically distinct, VSG. (
  • These "switchers" will then be recognized by the immune system, but not before another set of parasites will have turned on another VSG and escaped immune clearance. (
  • We think by studying these tactic new understandings about our immune system may be learned. (
  • T. solium also infects pigs, its intermediate host, leading to major economic losses [ 5 , 6 ]. (
  • Earning its title as the "ubiquitous parasite" it infects birds, sea and land mammals and can be found anywhere from the tropics of South America to the Svalbard islands of northern Norway . (
  • pyruvate generated by this is converted to lactate, a All the blood stages which account for all the human major source of the metabolic (lactic) acidosis seen pathology in malaria are haploid parasites. (
  • The host maximizes the distance between the epithelial cell layer and GI-inhabiting microbes to limit inflammation, and these strategies also likely keep bacteria out of the glands and crypts. (
  • However, the majority of infections are asymptomatic, possibly because the organism has co-evolved with its many vertebrate hosts and has developed multiple strategies to persist asymptomatically for the lifetime of the host. (
  • This finding gives important clues into a deadly parasite binding phenotype and could help explain why some malaria infections result in more severe complications than others. (
  • Infections are initiated by digestion of parasites deposited in cat feces or in undercooked meat. (
  • In most cases, chronic infections are largely asymptomatic unless the host becomes immune compromised. (
  • Many babesial parasites establish infections of long duration in immune hosts. (
  • In parasites, proteases are essential for host tissue degradation, immune evasion, and nutrition acquisition. (
  • Many of these eggs get lodged in host organs, such as the liver, resulting in chronic tissue damage. (
  • Splendore also identified this parasite in the tissue of a rabbit in 1908 ( 46 ). (
  • The presence of a tissue cyst (bradyzoite) life stage was rapidly recognized, but it was not until almost 60 years later that this organism was recognized to be a coccidian and that felines were identified as being the definitive hosts by several groups working independently, including Dubey and Frenkel in 1970 ( 16 ). (
  • Once tissue cysts or the environmental oocysts are ingested, their contents, the bradyzoites and sporozoites, respectively, invade host cells and differentiate into tachyzoites. (
  • The tissue-dwelling nematode Trichinella spiralis expresses paramyosin ( Ts Pmy) not only as a structural protein but also as an immunomodulator to alleviate complement attack by binding to some host complement components. (
  • The selected parasites show a distinct phenotype. (
  • Once inside, PfEMP1is expressed on the surface of RBCs that are infected with the mature stages of P. falciparum parasites. (
  • Within their mammalian hosts they often undergo extensive growth and differentiation with the ultimate goal of producing stages intended for transmission to the next intermediate host. (
  • In the case of B. bovis, this is accompanied by massive intravascular sequestration of infected red blood cells (IRBC) carrying mature parasite stages [10- 13]. (
  • In the present report, we have demonstrated the intracellular localization of this parasite-derived secreted serine protease and also its differential expression in virulent, avirulent, and attenuated strains of L. donovani as well as in different cell cycle stages of the parasite. (
  • Hosts, in turn, have evolved complex defences, with immune systems being among the most sophisticated processes known in nature. (
  • But parasites, too, have found their own ways to overcome defences and to manipulate their hosts for their own interests. (
  • The two forms, MTs and blood trypomastigotes use distinct sets of surface molecules to interact with their respective hosts. (
  • The team discovered an elevation of immune-dampening steroid molecules and a strong immunosuppressive signature in Gouin children. (
  • By contrasting correlative mechanistic evidence for host manipulation against rare cases of causative evidence and drawing from the advanced understanding of physiological systems from other disciplines it is clear we are often skipping over a crucial step in host-manipulation: the production, potential storage, and release of molecules (manipulation factors) that must create the observed physiological changes in hosts if they are adaptive. (
  • This increased enolase was enzymatically inactive and associated with the parasite membrane. (
  • It is secreted and can be found in the membrane of the parasite. (
  • P. falciparum erythrocyte membrane protein 1 (PfEMP-1), a variant surface antigen, has been shown to be anchored in these knobs and mediates adhesion to various host endothelial receptors. (
  • The protozoa, which cause malaria, depend on both cysteine and aspartic proteases to initiate host hemoglobin digestion. (
  • Eicosanoids in eukaryotic microbes appear to play a dual role, metabolism or maturation of the organism and communication with the host on a cellular basis. (
  • A parasite is an organism that needs a living host to survive. (
  • Hit and stay viruses evade immune control by sequestration, blockade of antigen presentation, cytokine escape, evasion of natural killer cell activities, escape from apoptosis, and antigenic change. (
  • This timely and up-to-date volume is essential reading for anyone working on kinetoplastid parasites and will also be of interest to parasitologists, immunologists and drug development researchers. (
  • The diseases caused by kinetoplastid parasites are neglected by the global expenditures in research and development, affecting millions of individuals in the low and middle-income countries located mainly in the tropical and subtropical regions. (
  • Domain analysis for the assembled dataset revealed families of serine, cysteine and proteinase inhibitors which might represent targets for parasite intervention. (
  • Potent proteolytic enzymes of cysteine, serine, and metalloprotease classes have been identified in secretory products of many of the parasites ( 8 , 19 , 26 , 27 , 30 ). (
  • CSI-Dublin facilitates integration of excellence in Immunology, Structural Biology, Medicinal Chemistry and Translational Medicine, creating a new interdisciplinary research platform targeted at drug discovery for immune-mediated diseases. (
  • A summary of the current ideas on the evolution of parasites, the impact of parasites on the evolution of their hosts and of the concept of host-parasite specificity will be presented and discussed. (
  • Claire M. Fraser, Ph.D., president and director of TIGR, said the institute's six years of research to help sequence the two malarial genomes represented only the first steps in its ambitious parasite genomics program. (
  • T. brucei periodically switches its variant surface glycoprotein (VSG) coat to evade host antibody clearance. (
  • It is an obligate intracellular parasite and cannot be propagated axenically. (
  • In this study, we showed that a distinct subset of parasites is selected on human brain endothelial cells and characterized the parasite ligands mediating cerebral binding. (
  • The results of these studies strongly suggested that fundamental changes had occurred in the antigenicity of protective antigen(s) in the surviving parasite populations, and demonstrated a probable association between recognition of the variant antigen and immune protection. (