A CC-type chemokine with specificity for CCR10 RECEPTORS. It is constitutively expressed in the skin and may play a role in T-CELL trafficking during cutaneous INFLAMMATION.
A CC-type chemokine with specificity for CCR7 RECEPTORS. It has activity towards DENDRITIC CELLS and T-LYMPHOCYTES.
A CC-type chemokine with specificity for CCR4 RECEPTORS. It has activity towards TH2 CELLS and TC2 CELLS.
A CC-type chemokine that is found at high levels in the THYMUS and has specificity for CCR4 RECEPTORS. It is synthesized by DENDRITIC CELLS; ENDOTHELIAL CELLS; KERATINOCYTES; and FIBROBLASTS.
A chemokine that is a chemoattractant for MONOCYTES and may also cause cellular activation of specific functions related to host defense. It is produced by LEUKOCYTES of both monocyte and lymphocyte lineage and by FIBROBLASTS during tissue injury. It has specificity for CCR2 RECEPTORS.
A CC-type chemokine with specificity for CCR7 RECEPTORS. It has activity towards T LYMPHOCYTES and B LYMPHOCYTES.
A CC-type chemokine that is a chemoattractant for EOSINOPHILS; MONOCYTES; and LYMPHOCYTES. It is a potent and selective eosinophil chemotaxin that is stored in and released from PLATELETS and activated T-LYMPHOCYTES. Chemokine CCL5 is specific for CCR1 RECEPTORS; CCR3 RECEPTORS; and CCR5 RECEPTORS. The acronym RANTES refers to Regulated on Activation, Normal T Expressed and Secreted.
A CC-type chemokine with specificity for CCR6 RECEPTORS. It has activity towards DENDRITIC CELLS; T-LYMPHOCYTES; and B-LYMPHOCYTES.
A CC-type chemokine secreted by activated MONOCYTES and T-LYMPHOCYTES. It has specificity for CCR8 RECEPTORS.
Group of chemokines with adjacent cysteines that are chemoattractants for lymphocytes, monocytes, eosinophils, basophils but not neutrophils.
Cell surface glycoproteins that bind to chemokines and thus mediate the migration of pro-inflammatory molecules. The receptors are members of the seven-transmembrane G protein-coupled receptor family. Like the CHEMOKINES themselves, the receptors can be divided into at least three structural branches: CR, CCR, and CXCR, according to variations in a shared cysteine motif.
A CC chemokine with specificity for CCR1 RECEPTORS and CCR5 RECEPTORS. It is a chemoattractant for NK CELLS; MONOCYTES; and a variety of other immune cells. This chemokine is encoded by multiple genes.
A monocyte chemoattractant protein that has activity towards a broad variety of immune cell types. Chemokine CCL7 has specificity for CCR1 RECEPTORS; CCR2 RECEPTORS; and CCR5 RECEPTORS.
Class of pro-inflammatory cytokines that have the ability to attract and activate leukocytes. They can be divided into at least three structural branches: C; (CHEMOKINES, C); CC; (CHEMOKINES, CC); and CXC; (CHEMOKINES, CXC); according to variations in a shared cysteine motif.
CCR receptors with specificity for CHEMOKINE CCL27. They may play a specialized role in the cutaneous homing of LYMPHOCYTES.
A CC chemokine with specificity for CCR5 RECEPTORS. It is a chemoattractant for NK CELLS; MONOCYTES and a variety of other immune cells. This chemokine is encoded by multiple genes.
A CXC chemokine that is chemotactic for T-LYMPHOCYTES and MONOCYTES. It has specificity for CXCR4 RECEPTORS. Two isoforms of CXCL12 are produced by alternative mRNA splicing.
CCR receptors with specificity for a broad variety of CC CHEMOKINES. They are expressed at high levels in MONOCYTES; tissue MACROPHAGES; NEUTROPHILS; and EOSINOPHILS.
A CXC chemokine that is induced by GAMMA-INTERFERON and is chemotactic for MONOCYTES and T-LYMPHOCYTES. It has specificity for the CXCR3 RECEPTOR.
A monocyte chemoattractant protein that attracts MONOCYTES; LYMPHOCYTES; BASOPHILS; and EOSINOPHILS. Chemokine CCL8 has specificity for CCR3 RECEPTORS and CCR5 RECEPTORS.
Chemokine receptors that are specific for CC CHEMOKINES.
CCR receptors with specificity for CHEMOKINE CCL2 and several other CCL2-related chemokines. They are expressed at high levels in T-LYMPHOCYTES; B-LYMPHOCYTES; MACROPHAGES; BASOPHILS; and NK CELLS.
A CC-type chemokine that is specific for CCR3 RECEPTORS. It is a potent chemoattractant for EOSINOPHILS.
A CC-type chemokine with specificity for CCR3 RECEPTORS. It is a chemoattractant for EOSINOPHILS.
CCR receptors with specificity for CHEMOKINE CCL19 and CHEMOKINE CCL21. They are expressed at high levels in T-LYMPHOCYTES; B-LYMPHOCYTES; and DENDRITIC CELLS.
CCR receptors with specificity for CHEMOKINE CCL1. They are expressed at high levels in T-LYMPHOCYTES; B-LYMPHOCYTES; and MACROPHAGES.
A CXC chemokine with specificity for CXCR2 RECEPTORS. It has growth factor activities and is implicated as a oncogenic factor in several tumor types.
The movement of leukocytes in response to a chemical concentration gradient or to products formed in an immunologic reaction.
CCR receptors with specificity for CHEMOKINE CCL17 and CHEMOKINE CCL22. They are expressed at high levels in T-LYMPHOCYTES; MAST CELLS; DENDRITIC CELLS; and NK CELLS.
Group of chemokines with paired cysteines separated by a different amino acid. CXC chemokines are chemoattractants for neutrophils but not monocytes.
A CX3C chemokine that is a transmembrane protein found on the surface of cells. The soluble form of chemokine CX3CL1 can be released from cell surface by proteolysis and act as a chemoattractant that may be involved in the extravasation of leukocytes into inflamed tissues. The membrane form of the protein may also play a role in cell adhesion.
Heparin-binding proteins that exhibit a number of inflammatory and immunoregulatory activities. Originally identified as secretory products of MACROPHAGES, these chemokines are produced by a variety of cell types including NEUTROPHILS; FIBROBLASTS; and EPITHELIAL CELLS. They likely play a significant role in respiratory tract defenses.
CCR receptors with specificity for CHEMOKINE CCL3; CHEMOKINE CCL4; and CHEMOKINE CCL5. They are expressed at high levels in T-LYMPHOCYTES; B-LYMPHOCYTES; MACROPHAGES; MAST CELLS; and NK CELLS. The CCR5 receptor is used by the HUMAN IMMUNODEFICIENCY VIRUS to infect cells.
CCR receptors with specificity for CHEMOKINE CCL11 and a variety of other CC CHEMOKINES. They are expressed at high levels in T-LYMPHOCYTES; EOSINOPHILS; BASOPHILS; and MAST CELLS.
An INTEFERON-inducible CXC chemokine that is specific for the CXCR3 RECEPTOR.
The movement of cells from one location to another. Distinguish from CYTOKINESIS which is the process of dividing the CYTOPLASM of a cell.
A CXC chemokine that is synthesized by activated MONOCYTES and NEUTROPHILS. It has specificity for CXCR2 RECEPTORS.
A CXC chemokine that is chemotactic for B-LYMPHOCYTES. It has specificity for CXCR5 RECEPTORS.
CXCR receptors with specificity for CXCL12 CHEMOKINE. The receptors may play a role in HEMATOPOIESIS regulation and can also function as coreceptors for the HUMAN IMMUNODEFICIENCY VIRUS.
A CXC chemokine that is induced by GAMMA-INTERFERON. It is a chemotactic factor for activated T-LYMPHOCYTES and has specificity for the CXCR3 RECEPTOR.
The movement of cells or organisms toward or away from a substance in response to its concentration gradient.
A CXC chemokine that has stimulatory and chemotactic activities towards NEUTROPHILS. It has specificity for CXCR1 RECEPTORS and CXCR2 RECEPTORS.
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.
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).
A CXC chemokine that is predominantly expressed in EPITHELIAL CELLS. It has specificity for the CXCR2 RECEPTORS and is involved in the recruitment and activation of NEUTROPHILS.
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.
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.
CXCR receptors that are expressed on the surface of a number of cell types, including T-LYMPHOCYTES; NK CELLS; DENDRITIC CELLS; and a subset of B-LYMPHOCYTES. The receptors are activated by CHEMOKINE CXCL9; CHEMOKINE CXCL10; and CHEMOKINE CXCL11.
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.
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.)
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.
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.
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.
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.
A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.
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.
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.
High-affinity G-protein-coupled receptors for INTERLEUKIN-8 present on NEUTROPHILS; MONOCYTES; and T-LYMPHOCYTES. These receptors also bind several other CXC CHEMOKINES.
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.
A chronic inflammatory genetically determined disease of the skin marked by increased ability to form reagin (IgE), with increased susceptibility to allergic rhinitis and asthma, and hereditary disposition to a lowered threshold for pruritus. It is manifested by lichenification, excoriation, and crusting, mainly on the flexural surfaces of the elbow and knee. In infants it is known as infantile eczema.
Established cell cultures that have the potential to propagate indefinitely.
A positive 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.
Chemokines that are chemoattractants for monocytes. These CC chemokines (cysteines adjacent) number at least three including CHEMOKINE CCL2.
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.
The outer covering of the body that protects it from the environment. It is composed of the DERMIS and the EPIDERMIS.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
A member of the CXC chemokine family that plays a role in the regulation of the acute inflammatory response. It is secreted by variety of cell types and induces CHEMOTAXIS of NEUTROPHILS and other inflammatory cells.
A molecule that binds to another molecule, used especially to refer to a small molecule that binds specifically to a larger molecule, e.g., an antigen binding to an antibody, a hormone or neurotransmitter binding to a receptor, or a substrate or allosteric effector binding to an enzyme. Ligands are also molecules that donate or accept a pair of electrons to form a coordinate covalent bond with the central metal atom of a coordination complex. (From Dorland, 27th ed)
CCR receptors with specificity for CHEMOKINE CCL20. They are expressed at high levels in T-LYMPHOCYTES; B-LYMPHOCYTES; and DENDRITIC CELLS.
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.
High-affinity G-protein-coupled receptors for INTERLEUKIN-8 present on NEUTROPHILS; MONOCYTES; and BASOPHILS.
They are oval or bean shaped bodies (1 - 30 mm in diameter) located along the lymphatic system.
Chemokine receptors that are specific for CXC CHEMOKINES.
A cell line derived from cultured tumor cells.
Ubiquitous, inducible, nuclear transcriptional activator that binds to enhancer elements in many different cell types and is activated by pathogenic stimuli. The NF-kappa B complex is a heterodimer composed of two DNA-binding subunits: NF-kappa B1 and relA.
A solvent for oils, fats, lacquers, varnishes, rubber waxes, and resins, and a starting material in the manufacturing of organic compounds. Poisoning by inhalation, ingestion or skin absorption is possible and may be fatal. (Merck Index, 11th ed)
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
Cell surface proteins that bind cytokines and trigger intracellular changes influencing the behavior of cells.
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 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.
Group of chemokines with the first two cysteines separated by three amino acids. CX3C chemokines are chemotactic for natural killer cells, monocytes, and activated T-cells.
CXCR receptors isolated initially from BURKITT LYMPHOMA cells. CXCR5 receptors are expressed on mature, recirculating B-LYMPHOCYTES and are specific for CHEMOKINE CXCL13.
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.
Chemical substances that attract or repel cells. The concept denotes especially those factors released as a result of tissue injury, microbial invasion, or immunologic activity, that attract LEUKOCYTES; MACROPHAGES; or other cells to the site of infection or insult.
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.
Highly specialized EPITHELIAL CELLS that line the HEART; BLOOD VESSELS; and lymph vessels, forming the ENDOTHELIUM. They are polygonal in shape and joined together by TIGHT JUNCTIONS. The tight junctions allow for variable permeability to specific macromolecules that are transported across the endothelial layer.
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.
Soluble mediators of the immune response that are neither antibodies nor complement. They are produced largely, but not exclusively, by monocytes and macrophages.
Cellular receptors that bind the human immunodeficiency virus that causes AIDS. Included are CD4 ANTIGENS, found on T4 lymphocytes, and monocytes/macrophages, which bind to the HIV ENVELOPE PROTEIN GP120.
A blood group consisting mainly of the antigens Fy(a) and Fy(b), determined by allelic genes, the frequency of which varies profoundly in different human groups; amorphic genes are common.
Cytotaxins liberated from normal or invading cells that specifically attract eosinophils; they may be complement fragments, lymphokines, neutrophil products, histamine or other; the best known is the tetrapeptide ECF-A, released mainly by mast cells.
The diffusion or accumulation of neutrophils in tissues or cells in response to a wide variety of substances released at the sites of inflammatory reactions.
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.
Ring compounds having atoms other than carbon in their nuclei. (Grant & Hackh's Chemical Dictionary, 5th ed)
Either of the pair of organs occupying the cavity of the thorax that effect the aeration of the blood.
White blood cells. These include granular leukocytes (BASOPHILS; EOSINOPHILS; and NEUTROPHILS) as well as non-granular leukocytes (LYMPHOCYTES and MONOCYTES).
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
The endogenous compounds that mediate inflammation (AUTACOIDS) and related exogenous compounds including the synthetic prostaglandins (PROSTAGLANDINS, SYNTHETIC).
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.
Subset of helper-inducer T-lymphocytes which synthesize and secrete the interleukins IL-4, IL-5, IL-6, and IL-10. These cytokines influence B-cell development and antibody production as well as augmenting humoral responses.
Phenomenon of cell-mediated immunity measured by in vitro inhibition of the migration or phagocytosis of antigen-stimulated LEUKOCYTES or MACROPHAGES. Specific CELL MIGRATION ASSAYS have been developed to estimate levels of migration inhibitory factors, immune reactivity against tumor-associated antigens, and immunosuppressive effects of infectious microorganisms.
The type species of LENTIVIRUS and the etiologic agent of AIDS. It is characterized by its cytopathic effect and affinity for the T4-lymphocyte.
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.
Granular leukocytes with a nucleus that usually has two lobes connected by a slender thread of chromatin, and cytoplasm containing coarse, round granules that are uniform in size and stainable by eosin.
Regulatory proteins and peptides that are signaling molecules involved in the process of PARACRINE COMMUNICATION. They are generally considered factors that are expressed by one cell and are responded to by receptors on another nearby cell. They are distinguished from HORMONES in that their actions are local rather than distal.
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)
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 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.
Cells that line the inner and outer surfaces of the body by forming cellular layers (EPITHELIUM) or masses. Epithelial cells lining the SKIN; the MOUTH; the NOSE; and the ANAL CANAL derive from ectoderm; those lining the RESPIRATORY SYSTEM and the DIGESTIVE SYSTEM derive from endoderm; others (CARDIOVASCULAR SYSTEM and LYMPHATIC SYSTEM) derive from mesoderm. Epithelial cells can be classified mainly by cell shape and function into squamous, glandular and transitional epithelial cells.
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.
Adherence of cells to surfaces or to other cells.
Proteins prepared by recombinant DNA technology.
Subset of helper-inducer T-lymphocytes which synthesize and secrete interleukin-2, gamma-interferon, and interleukin-12. Due to their ability to kill antigen-presenting cells and their lymphokine-mediated effector activity, Th1 cells are associated with vigorous delayed-type hypersensitivity reactions.
Specialized tissues that are components of the lymphatic system. They provide fixed locations within the body where a variety of LYMPHOCYTES can form, mature and multiply. The lymphoid tissues are connected by a network of LYMPHATIC VESSELS.
A classification of T-lymphocytes, especially into helper/inducer, suppressor/effector, and cytotoxic subsets, based on structurally or functionally different populations of cells.
The determination of the pattern of genes expressed at the level of GENETIC TRANSCRIPTION, under specific circumstances or in a specific cell.
A CXC chemokine that is found in the alpha granules of PLATELETS. The protein has a molecular size of 7800 kDa and can occur as a monomer, a dimer or a tetramer depending upon its concentration in solution. Platelet factor 4 has a high affinity for HEPARIN and is often found complexed with GLYCOPROTEINS such as PROTEIN C.
Connective tissue cells of an organ found in the loose connective tissue. These are most often associated with the uterine mucosa and the ovary as well as the hematopoietic system and elsewhere.
Elements of limited time intervals, contributing to particular results or situations.
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.
Washing liquid obtained from irrigation of the lung, including the BRONCHI and the PULMONARY ALVEOLI. It is generally used to assess biochemical, inflammatory, or infection status of the lung.
The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.
A spectrum of clinical liver diseases ranging from mild biochemical abnormalities to ACUTE LIVER FAILURE, caused by drugs, drug metabolites, and chemicals from the environment.
Unbroken cellular lining (intima) of the lymph vessels (e.g., the high endothelial lymphatic venules). It is more permeable than vascular endothelium, lacking selective absorption and functioning mainly to remove plasma proteins that have filtered through the capillaries into the tissue spaces.
A technique of culturing mixed cell types in vitro to allow their synergistic or antagonistic interactions, such as on CELL DIFFERENTIATION or APOPTOSIS. Coculture can be of different types of cells, tissues, or organs from normal or disease states.

Anti-monocyte chemoattractant protein-1/monocyte chemotactic and activating factor antibody inhibits neointimal hyperplasia in injured rat carotid arteries. (1/4001)

Monocyte chemoattractant protein-1 (MCP-1)/monocyte chemotactic and activating factor (MCAF) has been suggested to promote atherogenesis. The effects of in vivo neutralization of MCP-1 in a rat model were examined in an effort to clarify the role of MCP-1 in the development of neointimal hyperplasia. Competitive polymerase chain reaction analysis revealed maximum MCP-1 mRNA expression at 4 hours after carotid arterial injury. Increased immunoreactivities of MCP-1 were also detected at 2 and 8 hours after injury. Either anti-MCP-1 antibody or nonimmunized goat IgG (10 mg/kg) was then administered every 12 hours to rats that had undergone carotid arterial injury. Treatment with 3 consecutive doses of anti-MCP-1 antibody within 24 hours (experiment 1) and every 12 hours for 5 days (experiment 2) significantly inhibited neointimal hyperplasia at day 14, resulting in a 27.8% reduction of the mean intima/media ratio (P<0.05) in experiment 1 and a 43.6% reduction (P<0.01) in experiment 2. This effect was still apparent at day 56 (55.6% inhibition; P<0.05). The number of vascular smooth muscle cells in the neointima at day 4 was significantly reduced by anti-MCP-1 treatment, demonstrating the important role of MCP-1 in early neointimal lesion formation. However, recombinant MCP-1 did not stimulate chemotaxis of vascular smooth muscle cells in an in vitro migration assay. These results suggest that MCP-1 promotes neointimal hyperplasia in early neointimal lesion formation and that neutralization of MCP-1 before, and immediately after, arterial injury may be effective in preventing restenosis after angioplasty. Further studies are needed to clarify the mechanism underlying the promotion of neointimal hyperplasia by MCP-1.  (+info)

Infection of human endothelial cells with Chlamydia pneumoniae stimulates transendothelial migration of neutrophils and monocytes. (2/4001)

We have previously shown that different isolates of Chlamydia pneumoniae display heterogeneity in the in vitro stimulation of chemokines and adhesion molecules from infected human endothelial cells. In the present study, we examined the ability of different isolates of C. pneumoniae to promote transendothelial migration of neutrophils and monocytes. Human umbilical vein endothelial cells (HUVEC) were infected with low (<15)-passage C. pneumoniae isolates A-03, PS-32, and BR-393 and high (>40)-passage isolates BAL-16, TW-183, and T-2634, and levels of neutrophil and monocyte transendothelial migration were determined following 24 h of infection. Compared to mock-infected controls, significant increases in neutrophil migration were observed in response to most C. pneumoniae isolates examined (P < 0.001). Levels of monocyte migration were significantly increased in response to TW-183 and T-2634 (P < 0.001). Serial passage (>40 times) of the three low-passage isolates in HEp-2 cell cultures prior to infection of HUVEC generally resulted in the promotion of higher levels of neutrophil and monocyte transendothelial migration. These findings were compatible with differences observed in the extent of interleukin-8 (IL-8) and monocyte chemotactic protein-1 (MCP-1) stimulation between low- and high-passage A-03, PS-32, and BR-393. As opposed to C. pneumoniae, infection with C. trachomatis L2 caused only a slight increase in neutrophil transendothelial migration, which correlated with the lack of measurable IL-8 levels by this species. However, significant levels of monocyte migration were induced in response to C. trachomatis L2 despite a lack of measurable MCP-1 stimulation. C. trachomatis serovars A and E also failed to induce IL-8 and MCP-1 production in HUVEC. Results from this study indicate that the passage history of C. pneumoniae may play a role in the divergence of stimulatory activities observed among isolates in human endothelial cells. In addition, the differences observed between this organism and C. trachomatis suggest that the upregulation of IL-8 and MCP-1 in endothelial cells may be unique to C. pneumoniae.  (+info)

Luteal regression in the normally cycling rat: apoptosis, monocyte chemoattractant protein-1, and inflammatory cell involvement. (3/4001)

In hypophysectomized rats, prolactin induces regression of the corpora lutea. Luteal regression is accompanied by infiltration of monocytes/macrophages, declines in luteal mass and plasma progestins, and increased staining for monocyte chemoattractant protein-1 (MCP-1). We investigated whether similar events are induced during the estrous cycle, after the proestrous prolactin surge. Rats were killed on proestrus or on estrus, and one ovary was frozen for immunohistochemical detection of MCP-1, monocytes/macrophages (ED1-positive), and differentiated macrophages (ED2-positive) and for in situ detection of apoptotic nuclei. Corpora lutea of the current (proestrus) or preceding (estrus) cycle were dissected from the ovaries of additional rats and frozen for the same analyses and for determination of total protein content. In sections of whole ovaries, intensity and distribution of MCP-1 staining were increased in corpora lutea of multiple ages on estrus as compared to proestrus, as were numbers of differentiated macrophages and apoptotic nuclei per high-power field. Sections of isolated corpora lutea showed these increases on estrus, and the number of monocytes/macrophages per high-power field was also significantly increased. Accompanying these inflammatory/immune events, the corpora lutea on estrus showed decreased weight and total protein per corpus luteum, as compared to corpora lutea on proestrus. These changes are consistent with a proposed role for prolactin in the initiation of luteal apoptosis and of a sequence of inflammatory/immune events that accompany regression of the rat corpus luteum during the normal estrous cycle.  (+info)

Induction of macrophage C-C chemokine expression by titanium alloy and bone cement particles. (4/4001)

Particulate wear debris is associated with periprosthetic inflammation and loosening in total joint arthroplasty. We tested the effects of titanium alloy (Ti-alloy) and PMMA particles on monocyte/macrophage expression of the C-C chemokines, monocyte chemoattractant protein-1 (MCP-1), monocyte inflammatory protein-1 alpha (MIP-1alpha), and regulated upon activation normal T expressed and secreted protein (RANTES). Periprosthetic granulomatous tissue was analysed for expression of macrophage chemokines by immunohistochemistry. Chemokine expression in human monocytes/macrophages exposed to Ti-alloy and PMMA particles in vitro was determined by RT-PCR, ELISA and monocyte migration. We observed MCP-1 and MIP-1alpha expression in all tissue samples from failed arthroplasties. Ti-alloy and PMMA particles increased expression of MCP-1 and MIP-1alpha in macrophages in vitro in a dose- and time-dependent manner whereas RANTES was not detected. mRNA signal levels for MCP-1 and MIP-1alpha were also observed in cells after exposure to particles. Monocyte migration was stimulated by culture medium collected from macrophages exposed to Ti-alloy and PMMA particles. Antibodies to MCP-1 and MIP-1alpha inhibited chemotactic activity of the culture medium samples. Release of C-C chemokines by macrophages in response to wear particles may contribute to chronic inflammation at the bone-implant interface in total joint arthroplasty.  (+info)

Human immunodeficiency virus replication induces monocyte chemotactic protein-1 in human macrophages and U937 promonocytic cells. (5/4001)

We have recently described a significant correlation between human immunodeficiency virus-1 (HIV-1) RNA replication and monocyte chemotactic protein-1 (MCP-1) levels in the cerebrospinal fluid (CSF) of individuals with the acquired immunodeficiency syndrome (AIDS) with HIV encephalitis (E). Because local macrophages (microglia) are the cells predominantly infected in the brain, we investigated whether in vitro HIV infection affects MCP-1 production in mononuclear phagocytes (MP). MCP-1 secretion and expression were consinstently upregulated over constitutive levels in human monocyte-derived macrophages (MDM) infected with the M-tropic R5 BaL strain of HIV-1. HIV replication was required for this effect, as demonstrated by the absence of chemokine upregulation after infection in the presence of 3'-azido-3'-deoxythimidine (AZT) or cell-exposure to heat-inactivated (triangle up degrees ) virus. MCP-1 induction was not restricted to HIV-1 BaL, but was also observed during productive infection of MDM with two primary isolates differing for entry coreceptor usage and of U937 cells with the X4 HIV-1 MN strain. Based on the observation that exogenous HIV-1 Tat induced MCP-1 expression in astrocytes, we also investigated its role in MDM and U937 cells. Exogenous Tat induced MCP-1 production from MDM in a concentration-dependent manner, however, it was not effective on uninfected U937 cells or on the chronically infected U937-derived cell line U1. Transfection of Tat-expressing plasmids moderately activated HIV expression in U1 cells, but failed to induce MCP-1 expression in this cell line or in uninfected U937 cells. HIV replication-dependent expression of MCP-1 in MP may be of particular relevance for the pathogenesis of HIV infection in nonlymphoid organs such as the brain.  (+info)

Chemokine expression in CF epithelia: implications for the role of CFTR in RANTES expression. (6/4001)

To delineate the mechanisms that facilitate leukocyte migration into the cystic fibrosis (CF) lung, expression of chemokines, including interleukin-8 (IL-8), monocyte chemoattractant protein-1 (MCP-1), and RANTES, was compared between CF and non-CF airway epithelia. The findings presented herein demonstrate that, under either basal conditions or tumor necrosis factor-alpha (TNF-alpha)- and/or interferon-gamma (IFN-gamma)-stimulated conditions, a consistent pattern of differences in the secretion of IL-8 and MCP-1 between CF and non-CF epithelial cells was not observed. In contrast, CF epithelial cells expressed no detectable RANTES protein or mRNA under basal conditions or when stimulated with TNF-alpha and/or IFN-gamma (P +info)

Angiotensin II plays a pathogenic role in immune-mediated renal injury in mice. (7/4001)

Several lines of evidence show the importance of angiotensin II (AII) in renal injuries, especially when hemodynamic abnormalities are involved. To elucidate the role of AII in immune-mediated renal injury, we studied anti-glomerular basement membrane (GBM) nephritis in AII type 1a receptor (AT1a)-deficient homozygous (AT1a-/-) and wild-type (AT1a+/+) mice. A transient activation of the renin-angiotensin system (RAS) was observed in both groups of mice at around day 1. A renal expression of monocyte chemoattractant protein-1 (MCP-1) was transiently induced at six hours in both groups, which was then downregulated at day 1. In the AT1a+/+ mice, after RAS activation, the glomerular expression of MCP-1 was exacerbated at days 7 and 14. Thereafter, severe proteinuria developed, and the renal expressions of transforming growth factor-beta1 (TGF-beta1) and collagen type I increased, resulting in severe glomerulosclerosis and interstitial fibrosis. In contrast, glomerular expression of MCP-1, proteinuria, and tissue damage were markedly ameliorated in the AT1a-/- mice. Because this amelioration is likely due to the lack of AT1a, we can conclude that AII action, mediated by AT1a, plays a pathogenic role in anti-GBM nephritis, in which AII may contribute to the exacerbation of glomerular MCP-1 expression. These results suggest the involvement of AII in immune-mediated renal injuries.  (+info)

MCP-1 deficiency reduces susceptibility to atherosclerosis in mice that overexpress human apolipoprotein B. (8/4001)

The earliest recognizable atherosclerotic lesions are fatty streaks composed of lipid-laden macrophages (foam cells). Circulating monocytes are the precursors of these foam cells, but the molecular mechanisms that govern macrophage trafficking through the vessel wall are poorly understood. Monocyte chemoattractant protein-1 (MCP-1), a member of the chemokine (chemotactic cytokine) family, is a potent monocyte agonist that is upregulated by oxidized lipids. Recent studies in hypercholesterolemic mice lacking apo E or the low-density lipoprotein receptor have suggested a role for MCP-1 in monocyte recruitment to early atherosclerotic lesions. To determine if MCP-1 is critically involved in atherogenesis in the setting of elevated physiological plasma cholesterol levels, we deleted the MCP-1 gene in transgenic mice expressing human apo B. Here we report that the absence of MCP-1 provides dramatic protection from macrophage recruitment and atherosclerotic lesion formation in apo B transgenic mice, without altering lipoprotein metabolism. Taken together with the results of earlier studies, these data provide compelling evidence that MCP-1 plays a critical role in the initiation of atherosclerosis.  (+info)

There are several key features of inflammation:

1. Increased blood flow: Blood vessels in the affected area dilate, allowing more blood to flow into the tissue and bringing with it immune cells, nutrients, and other signaling molecules.
2. Leukocyte migration: White blood cells, such as neutrophils and monocytes, migrate towards the site of inflammation in response to chemical signals.
3. Release of mediators: Inflammatory mediators, such as cytokines and chemokines, are released by immune cells and other cells in the affected tissue. These molecules help to coordinate the immune response and attract more immune cells to the site of inflammation.
4. Activation of immune cells: Immune cells, such as macrophages and T cells, become activated and start to phagocytose (engulf) pathogens or damaged tissue.
5. Increased heat production: Inflammation can cause an increase in metabolic activity in the affected tissue, leading to increased heat production.
6. Redness and swelling: Increased blood flow and leakiness of blood vessels can cause redness and swelling in the affected area.
7. Pain: Inflammation can cause pain through the activation of nociceptors (pain-sensing neurons) and the release of pro-inflammatory mediators.

Inflammation can be acute or chronic. Acute inflammation is a short-term response to injury or infection, which helps to resolve the issue quickly. Chronic inflammation is a long-term response that can cause ongoing damage and diseases such as arthritis, asthma, and cancer.

There are several types of inflammation, including:

1. Acute inflammation: A short-term response to injury or infection.
2. Chronic inflammation: A long-term response that can cause ongoing damage and diseases.
3. Autoimmune inflammation: An inappropriate immune response against the body's own tissues.
4. Allergic inflammation: An immune response to a harmless substance, such as pollen or dust mites.
5. Parasitic inflammation: An immune response to parasites, such as worms or fungi.
6. Bacterial inflammation: An immune response to bacteria.
7. Viral inflammation: An immune response to viruses.
8. Fungal inflammation: An immune response to fungi.

There are several ways to reduce inflammation, including:

1. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs).
2. Lifestyle changes, such as a healthy diet, regular exercise, stress management, and getting enough sleep.
3. Alternative therapies, such as acupuncture, herbal supplements, and mind-body practices.
4. Addressing underlying conditions, such as hormonal imbalances, gut health issues, and chronic infections.
5. Using anti-inflammatory compounds found in certain foods, such as omega-3 fatty acids, turmeric, and ginger.

It's important to note that chronic inflammation can lead to a range of health problems, including:

1. Arthritis
2. Diabetes
3. Heart disease
4. Cancer
5. Alzheimer's disease
6. Parkinson's disease
7. Autoimmune disorders, such as lupus and rheumatoid arthritis.

Therefore, it's important to manage inflammation effectively to prevent these complications and improve overall health and well-being.

Also known as eczema or atopic eczema.

Dermatitis, Atopic is a common condition that affects people of all ages but is most prevalent in children. It is often associated with other atopic conditions such as asthma and allergies. The exact cause of dermatitis, atopic is not known, but it is thought to involve a combination of genetic and environmental factors.

Symptoms of Dermatitis, Atopic:

* Redness and dryness of the skin
* Scaling and flaking of the skin
* Itching and burning sensations
* Thickening and pigmentation of the skin
* Small blisters or weeping sores

Atopic dermatitis can occur anywhere on the body but is most commonly found on the face, neck, hands, and feet.

Treatment for Dermatitis, Atopic:

* Moisturizers to keep the skin hydrated and reduce dryness
* Topical corticosteroids to reduce inflammation
* Antihistamines to relieve itching
* Phototherapy with ultraviolet light
* Oral immunomodulators for severe cases

It is important to note that dermatitis, atopic is a chronic condition, and treatment should be ongoing. Flare-ups may occur, and adjustments to the treatment plan may be necessary.

Prevention of Dermatitis, Atopic:

* Avoiding triggers such as soaps, detergents, and stress
* Keeping the skin well-moisturized
* Avoiding extreme temperatures and humidity
* Wearing soft, breathable clothing
* Using mild cleansers and avoiding harsh chemicals

Early diagnosis and treatment of dermatitis, atopic can help improve the quality of life for those affected. It is important to work with a healthcare professional to develop an appropriate treatment plan and manage symptoms effectively.

1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.

2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.

3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.

4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.

5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.

6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.

7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.

8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.

9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.

10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.

The symptoms of carbon tetrachloride poisoning can vary depending on the level and duration of exposure, but may include:

* Respiratory problems, such as coughing, wheezing, and shortness of breath
* Nausea and vomiting
* Abdominal pain and diarrhea
* Headaches and dizziness
* Confusion and disorientation
* Slurred speech and loss of coordination
* Seizures and coma

If you suspect that you or someone else has been exposed to carbon tetrachloride, it is essential to seek medical attention immediately. Treatment for carbon tetrachloride poisoning typically involves supportive care, such as oxygen therapy and hydration, as well as medications to manage symptoms and remove the toxin from the body. In severe cases, hospitalization may be necessary.

Prevention is key when it comes to carbon tetrachloride poisoning. If you work with or are exposed to CTC, it is important to take safety precautions such as wearing protective clothing and equipment, using proper ventilation, and following all safety protocols. It is also essential to handle the chemical with care and store it in a safe location.

In conclusion, carbon tetrachloride poisoning can be a serious and potentially deadly condition that requires immediate medical attention. If you suspect exposure to CTC, it is crucial to seek medical help right away. By taking safety precautions and being aware of the risks associated with this chemical, you can prevent carbon tetrachloride poisoning and protect your health.

The definition of DILI has been revised several times over the years, but the most recent definition was published in 2013 by the International Consortium for DILI Research (ICDCR). According to this definition, DILI is defined as:

"A clinically significant alteration in liver function that is caused by a medication or other exogenous substance, and is not related to underlying liver disease. The alteration may be biochemical, morphological, or both, and may be acute or chronic."

The ICDCR definition includes several key features of DILI, including:

1. Clinically significant alteration in liver function: This means that the liver damage must be severe enough to cause symptoms or signs of liver dysfunction, such as jaundice, nausea, vomiting, or abdominal pain.
2. Caused by a medication or other exogenous substance: DILI is triggered by exposure to certain drugs or substances that are not related to underlying liver disease.
3. Not related to underlying liver disease: This means that the liver damage must not be caused by an underlying condition such as hepatitis B or C, alcoholic liver disease, or other genetic or metabolic disorders.
4. May be acute or chronic: DILI can occur as a sudden and severe injury (acute DILI) or as a slower and more insidious process (chronic DILI).

The ICDCR definition provides a standardized way of defining and diagnosing DILI, which is important for clinicians and researchers to better understand the cause of liver damage in patients who are taking medications. It also helps to identify the drugs or substances that are most likely to cause liver injury and to develop strategies for preventing or treating DILI.

The CCL2 chemokine is also expressed by neurons, astrocytes and microglia. The expression of CCL2 in neurons is mainly found in ... CCL2 is a small cytokine that belongs to the CC chemokine family. CCL2 tightly regulates cellular mechanics and thereby ... CCL2 and many other CC chemokines are located on chromosome 17 (17q11.2-q21.1). The gene span is 1,927 bases and the CCL2 gene ... The chemokine (C-C motif) ligand 2 (CCL2) is also referred to as monocyte chemoattractant protein 1 (MCP1) and small inducible ...
Typical inflammatory chemokines include: CCL2, CCL3 and CCL5, CXCL1, CXCL2 and CXCL8. A typical example is CXCL-8, which acts ... C4-CC chemokines), but a small number of CC chemokines possess six cysteines (C6-CC chemokines). C6-CC chemokines include CCL1 ... The third group of chemokines is known as the C chemokines (or γ chemokines), and is unlike all other chemokines in that it has ... CCL1 for the ligand 1 of the CC-family of chemokines, and CCR1 for its respective receptor. The CC chemokine (or β-chemokine) ...
Ways include chemokine CCL2 nitration, which traps T cells in the stroma. Tumor vasculature helps tumors preferentially recruit ...
Tomczak A, Pisabarro MT (April 2011). "Identification of CCR2-binding features in Cytl1 by a CCL2-like chemokine model". ...
5-Oxo-ETE also acts in synergy with two chemokines, CCL2 and CCL8, in stimulating monocyte chemotaxis. The interactions of 5- ... and the two CCL chemokines) in neutrophils and monocytes further suggest that it plays a role in inflammatory responses and ...
This receptor has several CC chemokine ligands including CCL2, CCL3, CCL4, CCL5, CCL11, CCL13, CCL14 and CCL16. CCR6, a ... The CC chemokine receptors all work by activating the G protein Gi. CCR1 was the first CC chemokine receptor identified and ... CC chemokine receptors (or beta chemokine receptors) are integral membrane proteins that specifically bind and respond to ... May 1997). "Molecular cloning of a novel human CC chemokine EBI1-ligand chemokine that is a specific functional ligand for EBI1 ...
L-RNA aptamers have been obtained for the chemokines CCL2 and CXCL12, the complement components C5a and ghrelin. They are ... Proof-of-concept for an anti-CCL2/MCP-1 L-RNA aptamers has recently been demonstrated in diabetic nephropathy patients. They ...
"Atypical Chemokine Receptor ACKR2-V41A Has Decreased CCL2 Binding, Scavenging, and Activation, Supporting Sustained ...
November 2015). "Differential Roles of Chemokines CCL2 and CCL7 in Monocytosis and Leukocyte Migration during West Nile Virus ... Power CA, Clemetson JM, Clemetson KJ, Wells TN (August 1995). "Chemokine and chemokine receptor mRNA expression in human ... Griffith JW, Sokol CL, Luster AD (2014). "Chemokines and chemokine receptors: positioning cells for host defense and immunity ... October 1998). "HIV-1 envelope gp120 inhibits the monocyte response to chemokines through CD4 signal-dependent chemokine ...
This gene encodes two isoforms of a receptor for monocyte chemoattractant protein-1 (CCL2), a chemokine which specifically ... CCR2 is a CC chemokine receptor. This CCR2 gene is located in the chemokine receptor gene cluster region. Two alternatively ... "Entrez Gene: CCR2 chemokine (C-C motif) receptor 2". El Khoury J, Toft M, Hickman SE, Means TK, Terada K, Geula C, Luster AD ( ... C-C chemokine receptor type 2 (CCR2 or CD192 (cluster of differentiation 192) is a protein that in humans is encoded by the ...
... due to the chemokine CCL2 in rat skin. A similar effect was observed using Lipopolysaccharide (LPS) instead of CCL2 ( ... Peptide 3' is a 12-amino acid linear peptide corresponding to amino acids 51 to 62 of mature human chemokine CCL2. It is formed ... When the 12-amino acid sequence of 'peptide 3'/CCL2 is aligned with the sequences of the other chemokines CCL3, CXCL8 and ... Ala4 in CCL2 is also present in CCL3 but the corresponding residue is Leu in CXCL8 and Ile in CXCL12. Inclusion of Leu at ...
These chemokines include CCL11, CCL2 and CCL12, which are highly localized on mouse and human chromosomes, implicating a ... In healthy aging humans, the plasma and cerebrospinal fluid levels of certain chemokines are elevated. In a mouse model, plasma ... levels of these chemokines correlate with reduced neurogenesis, suggesting that neurogenesis may be modulated by certain global ...
... host-derived pro-inflammatory chemokines (e.g. CXCL8, CCL2, CCL3, CCL4, CCL5, CCL11, CXCL10), platelet-activating factor, and ... stimulates their expression the chemokine receptor, CCR5, to inhibit chemokine signaling, enhances their phagocyte activity, ... CMKLR1 (chemokine receptor-like 1), also termed the ChemR23 or E series resolvin receptor (ERV), is expressed on inflammation- ...
These factors include most particularly chemokines such as monocyte chemotactic protein-1 (CCL2) and monocyte chemotactic ... "Single-cell analysis reveals chemokine-mediated differential regulation of monocyte mechanics". iScience. 25 (1): 103555. ...
June 2013). "Phase 2 study of carlumab (CNTO 888), a human monoclonal antibody against CC-chemokine ligand 2 (CCL2), in ... October 2013). "Utilizing pharmacokinetics/pharmacodynamics modeling to simultaneously examine free CCL2, total CCL2 and ... an Anti-Chemokine Ligand 2 [CCL2]) in Participants With Metastatic Castrate-Resistant Prostate Cancer" at ClinicalTrials.gov ... that targets human CC chemokine ligand 2 (CCL2)/monocyte chemoattractant protein (MCP1). Carlumab was under development for use ...
NOX-A12 targets CXCL12 (C-X-C Chemokine Ligand 12), a key chemokine protein. Favorable results were reported in October 2018 ... NOX-E36 targets MCP-1, also called CCL2. A third Spiegelmer (NOX-H94, lexaptepid pegol) has been in a clinical trial for the ...
It has been used to demonstrate the role of TRPM2 in immune system function, both triggering release of the chemokine CCL2 from ... November 2018). "Selective agonist of TRPML2 reveals direct role in chemokine release from innate immune cells". eLife. 7. doi: ...
CCL2 and CCL7. PAR1 is inhibited by Vorapaxar when the molecule binds to a binding pocket between extracellular loop 2 and 3 of ... inflammatory response to Streptococcus pneumoniae by reducing levels of pro-inflammatory cytokines such as IL-1β and chemokines ...
The observation that the chemokine CCL2 is potentially responsible for the recruitment of macrophages to atherosclerotic ... A broad-spectrum chemokine inhibitor or BSCI (also termed chemotide or somatotaxin ) is a type of experimental anti- ... Grainger DJ, Reckless J, Fox DJ (2005). "Broad Spectrum Chemokine Inhibitors Related to NR58-3.14.3". Mini-Rev. Med. Chem. 5 (9 ... Kayisli UA, Berkkanoglu M, Zhang L, Kizilay G, Arici A (2007). "The Broad-Spectrum Chemokine Inhibitor NR58-3.14.3 Suppresses ...
... which induces chemokines such as CCL2 and CCL20 independently of IRF3. STING is also thought to activate the NF-κB ...
Recent work has also determined that genetic and pharmacologic targeting of chemokine (C-C motif) ligand 2 (CCL2) also known as ...
One study showed that monocyte chemotactic protein-1 (chemokine CCL-2) and neutrophil gelatinase associated lipocalin (NGAL) ...
CCL2 (MCP-1) CCL4 (MIP-1) CCL5 (RANTES) CCL17 (TARC) CCL22 (Macrophage-derived chemokine) Chemokines are a group of small ... "Macrophage-derived chemokine is a functional ligand for the CC chemokine receptor 4". J. Biol. Chem. 273 (3): 1764-8. doi: ... "The T cell-directed CC chemokine TARC is a highly specific biological ligand for CC chemokine receptor 4". J. Biol. Chem. 272 ( ... C-C chemokine receptor type 4 is a protein that in humans is encoded by the CCR4 gene. CCR4 has also recently been designated ...
... and chemokine (C-C motif) ligand 2 (CCL2), all of which are occupied in chemotactic pathways involved in leukocyte recruitment ...
The study showed that mice lacking MR1 had a significantly decreased transcript level of cytokines/chemokines known to be ... associated with inflammation, such as Ccl2, Ccl5, Il1β, Il6, Il17a, Ifnγ, and Tnfα. In contrast, the transcript level of ...
Cantuzumab ravtansine Cathelicidin CC chemokine receptors CCBP2 CCL1 CCL11 CCL12 CCL13 CCL14 CCL15 CCL16 CCL17 CCL18 CCL19 CCL2 ... Breakthrough infection Broadly neutralizing HIV-1 antibodies Bursa of Fabricius C-C chemokine receptor type 6 C-C chemokine ... CD4 CD4+ T cells and antitumor immunity CD74 CD94/NKG2 Cell-mediated immunity CELSR1 Central tolerance Chemokine Chemokine ... CR6261 CroFab Cross-presentation Cross-reactivity Cryptic self epitopes Cryptotope CX3CL1 CX3CR1 CXC chemokine receptors CXCL1 ...
N-CCL2), which traps T cells in the stroma of colon and prostate cancers. N-CCL2 does attract monocytes. CCL2 nitration ... For instance, inhibiting chemokine receptor type 2 (CCR2), colony-stimulating factor-1 receptor (CSF-1R) and granulocyte ... In a preclinical PDA mouse model, FAP+ CAFs produced the chemokine CXCL12, which is bound by PDA cancer cells. Because FAP+ ... One such mechanism is the release of cell-type specific chemokines. Another is the TME's capacity to posttranslationally alter ...
... causes CCL2 secretion to be lowered, and thus the mobility of monocytes to be reduced. This explains part of the ... It was shown that while deoxynivalenol induces the secretion of chemokines, which are also immunorelevant messenger molecules, ... Another important factor influenced by nivalenol is MCP-1/CCL2, this cytokine plays a role in the mobility regulation of ...
2008). "Macrophage-specific metalloelastase (MMP-12) truncates and inactivates ELR+ CXC chemokines and generates CCL2, -7, -8, ... "Entrez Gene: chemokine (C-C motif) ligand 8". Van Coillie E, Fiten P, Nomiyama H, Sakaki Y, Miura R, Yoshie O, Van Damme J, ... Chemokine (C-C motif) ligand 8 (CCL8), also known as monocyte chemoattractant protein 2 (MCP2), is a protein that in humans is ... The gene for CCL8 is encoded by 3 exons and is located within a large cluster of CC chemokines on chromosome 17q11.2 in humans ...
In addition to other chemokines, such as CCL2, CCL3, and CCL4, the presence of CCL1 has been reported in the development of ... Chemokine (C-C motif) ligand 1 (CCL1) is also known as small inducible cytokine A1 and I-309 in humans. CCL1 is a small ... CCL1 is encoded by CCL1 gene which is one of the several chemokine genes clustered on the chromosome 17q11.2-q12 in humans. It ... July 1998). "The chemokine receptor CCR8 is preferentially expressed in Th2 but not Th1 cells". Journal of Immunology. 161 (2 ...
It induces the expression of pro-inflammatory genes such as CXCL-1, CCL2, and IL-1 and inhibits anti-inflammatory genes such as ... This specific population can produce chemokines to mediate the infiltration of neutrophils in an inflammatory response. Dermal ... When under physical stress, the release of CCL2 (cytokine) in the hair follicle induces the infiltration of macrophages. The ... a pathway responding to chemokines. The infiltration of circulating monocytes can also be triggered through the upregulation of ...
Similar to psoriasin, mS100a7a15 recruits leukocytes and induces proinflammatory chemokines as well as cytokines in ... angiogenesis and metastasis through induction of prometastatic and angiogenic factors like CCL2, Cox-2, MMP2, MMP9 and VEGF. ...
The SASP cytokine CCL2 (MCP1) recruits macrophages to remove cancer cells. Although transient expression of SASP can recruit ... SASP may also consist of exosomes and ectosomes containing enzymes, microRNA, DNA fragments, chemokines, and other bioactive ... Cancer invasiveness is promoted primarily though the actions of the SASP factors metalloproteinase, chemokine, interleukin 6 ( ... "Chemokine signaling via the CXCR2 receptor reinforces senescence". Cell. 133 (6): 1006-18. doi:10.1016/j.cell.2008.03.038. PMID ...
Circulating leukocytes are localised towards the site of injury or infection due to the presence of chemokines.[citation needed ... CCL2 has a similar function to CXCL8, inducing monocyte extravasation and development into macrophages); also activates ... This is assisted through juxtacrine activation of integrins by chemokines and soluble factors released by endothelial cells. In ... TNFα and chemokines. IL-1, TNFα and C5a cause the endothelial cells of blood vessels near the site of infection to express ...
STING may play an important role in the production of MCP-1 and CCL7 chemokines. STING deficient monocytes are intrinsically ... CCL2, CCL20, etc. Several reports suggested that STING is associated with the activation of selective autophagy. Mycobacterium ...
... encoding protein Zinc finger protein 830 Several CC chemokines: CCL1, CCL2, CCL3, CCL4, CCL5, CCL7, CCL8, CCL11, CCL13, CCL14, ... C-C motif chemokine ligand 4 like 1 (17q12) DDX52: DExD-box helicase 52 (17q12) ERBB2 loca leukemia viral oncogene homolog 2, ...
It mediates chemokine transcytosis, which leads to apical retention of intact chemokines and more leukocyte migration. Binding ... CCL2 regulated upon activation normal T expressed and secreted (RANTES) - CCL5 melanoma growth stimulatory activity (MSGA-α), ... "Expression of chemokines and chemokine receptors during human renal transplant rejection". Am. J. Kidney Dis. 37 (3): 518-31. ... Duffy Antigen Receptor for Chemokines). The chemokine binding site on the receptor appears to be localised to the amino ...
Chemokine ligands CXCL9, CXCL10, and CCL5 that bind to chemokine receptors such as CXCR3 and CCR5, Immune suppressive or ... Antigen-activated T cells secrete CCR5 ligands (CCL2 and CCL3) to recruit natural killer (NK) cells and other innate immune ... These initiate the following cascade: CXCR3 ligand chemokines (CXCL-9, -10 and -11) are produced in response to activated B ... To illustrate, growth factors and chemokines activated in response to injury are recruited by tumour cells, sustaining chronic ...
... particularly chemokines such as CXCL10 and CCL2 (MCP-1) which attract monocytes, natural killer cells, T-lymphocytes, and ... Keratinocytes also modulate the immune system: apart from the above-mentioned antimicrobial peptides and chemokines they are ...
"Neutrophil recruitment by human IL-17 via C-X-C chemokine release in the airways". Journal of Immunology. 162 (4): 2347-52. ... "IL-17RA is required for CCL2 expression, macrophage recruitment, and emphysema in response to cigarette smoke". PLOS ONE. 6 (5 ... "Cooperation of interleukin-17 and interferon-gamma on chemokine secretion in human fetal intestinal epithelial cells". Clinical ... "Requirement of interleukin 17 receptor signaling for lung CXC chemokine and granulocyte colony-stimulating factor expression, ...
Interplay between several molecules (cytokines, chemokines, proteases, and inflammatory mediators) culminates in causing damage ... CCL2: chemokine [c-c-motif] ligand-2/MCP1; CCL3: chemokine [c-c-motif] ligand-3/MIP-1; CXCL8: IL-8; LTB: TNF-C/induce ... c-c-motif receptor/beta chemokine receptor; CCL5: chemokine [c-c-motif] ligand-5/RANTES/its chemotactic for neutrophils; ... A. Krishnamurthy, V. Joshua, A. H. Hensvold et al., "Identification of a novel chemokine-dependent molecular mechanism ...
Chemokine. TNF. Interleukin. CCL2 (MCP-1). TNF (TNFα). IL-1α ... CCL2 (MCP-1), CCL3 (MIP-1α), CXCL9 (MIG), and CXCL10 (IP-10). ... The cytokines/chemokines included are implicated in inflammatory responses to disease states including autoimmune diseases, ... Human Qbeads Inflammation Panel Kit allows the measurement of seven human cytokines and chemokines from either serum or in ... Available for human, mouse, and rat secreted proteins including cytokines, chemokines, enzymes, and growth factors. ...
Ccl2. C-C motif chemokine ligand 2. increases expression. EXP. 2,4,6-trichlorophenyl 4-nitrophenyl ether results in increased ... expression of CCL2 mRNA; 2,4,6-trichlorophenyl 4-nitrophenyl ether results in increased expression of CCL2 protein. CTD. PMID: ...
Chemokine. CCL. *CCL1. *CCL2/MCP1. *CCL3/MIP1α. *CCL4/MIP1β. *CCL5/RANTES ...
High CSF and blood cytokine/chemokine (CXCL8/IL-8, CCL2/MCP-1, IL-6, CXCL10/IP-10) levels were detected. No evidence of direct ... We found a broader range of cytokines/chemokines being activated (7); for certain cytokines (CXCL8/IL-8, CCL2/MCP-1), the CSF ... Chemokines in the cerebrospinal fluid of patients with meningitis. Clin Immunol Immunopathol. 1996;80:155-61. DOIPubMedGoogle ... Chemokines and chemotaxis of leukocytes in infectious meningitis. J Neuroimmunol. 1998;85:33-43. DOIPubMedGoogle Scholar ...
q-PCR analysis of above metioned brain regions was used to measure the level of pro-inflammatory mediators such as; LIF, CCL2 ... Results revealed no significant increase of proinflammatory cytokine/chemokine expressions. However, significant downregulation ...
Chemokine CCL2 D12.644.276.374.200.110.500.600 D12.644.276.374.200.110.990.600. D12.776.467.374.200.110.500.600 D12.776.467.374 ... Replaced for 2008 by Chemokine CCL5). Raphe Nuclei A8.186.211.653.632. A8.186.211.865.507. Raynaud Disease C14.907.744 C14.907. ... Receptors, Chemokine D23.50.301.264.35.605. D23. Receptors, Complement 3b D23.50.301.264.35.600 D23.50.301.264. ...
The genes analysed were: interleukin 1β (Il1b), chemokine (C-C motif) ligand 2 (Ccl2) and intercellular adhesion molecule 1 ( ... 6d-f). Treatment of diabetic rats with 2-HDP caused a significant reduction in the mRNA levels of Ccl2, Il1b and Icam1 (Fig. 6d ... d-f) Column scatter graphs summarising retinal mRNA expression for the inflammatory signalling molecules Il1b (d), Ccl2 (e) and ... In line with our observation of increased numbers of activated microglia, the inflammatory markers Ccl2, Il1b and Icam1 were ...
Macrophage infiltration is directed by expression of chemokine (C-C motif) ligand 2 (CCL2 or MCP-1). CCL2 expression is ... Macrophage recruitment relies on chemoattractant proteins, such as monocyte chemoattractant protein (MCP)-1 or chemokine (C-C ... Adipose tissue microRNAs as regulators of CCL2 production in human obesity. Diabetes. 2012;. 61. (8):1986-1993. ... motif) ligand 2 (CCL2). The initial dose of MCP-1 release was found to be secreted by pre-adipocytes [129], supporting the ...
In summary, we provide a link between CCL2, CCR2 expression on macrophages, NADPH oxidase, ROS and the development CCL2- ... Local injection of neutrophilic chemokines elicits neutrophil recruitment but no hyperalgesia in rats. In meta-analyses the ... In Wistar rats, CCL2-induced hyperalgesia was completely blocked by superoxide dismutase (SOD), catalase or tempol. Likewise, ... In this study, intraplantar injection of CCL2 elicited thermal and mechanical pain in Wistar but not in Dark Agouti (DA) rats, ...
MicroRNA-495 regulates the proliferation and apoptosis of human umbilical vein endothelial cells by targeting chemokine CCL2. ...
The gene expression levels of six genes, namely serine palmitoyltransferase small subunit B (SPTSSB), C-C motif chemokine ... ligand 2 (CCL2), microsomal glutathione S-transferase 1 (MGST1), Dickkopf WNT signaling pathway inhibitor 1 (DKK1), sex- ...
1B). Expression levels of macrophage-attracting cytokines and chemokines CCL2, CCL19, and CCL21 were significantly higher in ... Cytokine and chemokine expression detection. Bead-based multiplex assay panel.. The supernatants of HT29 and SW480 cells, M1 ... As previously reported (34, 35), M2 macrophages secreted the chemokine CCL17, whereas colon cancer cells did not (Fig. 4A and ... Cytokines and chemokines involved in macrophage chemotaxis were significantly upregulated in ulcerative colitis and CACC ...
These included several CC chemokine ligands (CCLs; CCL20, CCL2 [also called SCYA2 or MCP-1]), CXC chemokine ligands (CXCLs; ... CXC chemokine receptors (CXCRs; CXCR2) and a recently characterized cytokine called chemokine-like factor 1 [19]. ... Shahrara S, Amin MA, Woods JM, Haines GK, Koch AE: Chemokine receptor expression and in vivo signaling pathways in the joints ... Schrier DJ, Schimmer RC, Flory CM, Tung DK, Ward PA: Role of chemokines and cytokines in a reactivation model of arthritis in ...
Snail on the other hand was found to modulate the secretion of chemokines, such as CXCL2, resulting in the increased ... CCL2, and CCL5; hence, recruiting tumor-associated macrophages (12). Additionally, Snail was found to induce regulatory T cells ... a chemokine that contributes to cancer metastasis as well as pro-tumorigenic immunomodulation (36), is upregulated in our GN25 ... reported to modulate interferon signaling and chemokines production to reduce inflammation (37). Another candidate found to ...
These NF- kappaB activated islets not only expressed the same chemokine profile observed in human islets, but also struggled to ... CCL2, CXCL12, CXCL1, CXCL6, CCL28. Of note, the inflammatory profile of isolated human islets was maintained after ... and notably high expression of a set of chemokines that would favour neutrophil and monocyte recruitment including CXCL2, ... and notably high expression of a set of chemokines that would favour neutrophil and monocyte recruitment including CXCL2, CCL2 ...
... it blocks migration of monocytes and granulocytes to inflammatory attracting factor CC-chemokine ligand 2 (CCL2) and macrophage ... Here, we report that CST blocks leukocyte migration towards inflammatory chemokines. By in vitro and in vivo migration assays, ...
... a set of inflammatory cytokines and chemokines, including TNF-α, CCL2 and CCL5 were elevated in Asxl1-/-Jak2VF mice compared ...
Chemokine CCL2 Entry term(s). CCL2 Chemokine CCL2, Chemokine CCL2, Chemokines Chemoattractant Protein-1, Monocyte Chemokine (C- ... Chimiokine CCL2 Entry term(s):. CCL2 Chemokine. CCL2, Chemokine. CCL2, Chemokines. Chemoattractant Protein-1, Monocyte. ... Chemokine (C-C Motif) Ligand 2. Chemokine, CCL2. Chemokines CCL2. Chemotactic Protein-1, Monocyte. Monocyte Chemoattractant ... Chemokine, CCL2 Chemokines CCL2 Chemotactic Protein-1, Monocyte Monocyte Chemoattractant Protein 1 Monocyte Chemoattractant ...
Voluntary exercise blocks Western diet-induced gene expression of the chemokines CXCL10 and CCL2 in the prefrontal cortex. ...
Cytokines and chemokines networks. The Kyoto Encyclopedia of Genes and Genomes (KEGG) was used to construct the chemokines and ... Chemoattractants, such as Cxcl2, Ccl2, Ccl3, Ccl4, and Ccl5, as well as pronounced inflammatory cytokine transcripts such as ... Most importantly, our conclusion regarding the chemokine and cytokine changes due to age does not change. The chemokine network ... Downregulation of the chemokines network due to age. Upper panel - Edges within the chemokine network in which both the ligand ...
The group found that chemokine CCL2 is significantly elevated in patients diagnosed with the rare form of cancer, and that the ... but which are also a source of chemokine CCL2, which are commonly found in the pleural effusions of mesothelioma patients, as ... It found that though CCL2 levels were elevated with the age of patients overall, there was a clear elevation of the protein in ... The more advanced the diseases stage, the higher the CCL2 levels. This gives researchers a specific target for future ...
Chemokine CCL2 Medicine & Life Sciences 65% * Eosinophils Medicine & Life Sciences 57% * Interleukin-5 Medicine & Life Sciences ... Eotaxin is one of the CC chemokines that selectively recruits eosinophils and contributes to the pathogenesis of allergic ... Eotaxin is one of the CC chemokines that selectively recruits eosinophils and contributes to the pathogenesis of allergic ... Eotaxin is one of the CC chemokines that selectively recruits eosinophils and contributes to the pathogenesis of allergic ...
Soria G, Ben-Baruch A. The inflammatory chemokines CCL2 and CCL5 in breast cancer. Cancer Lett. 2008;267(2):271-85. doi:10.1016 ... CCL2-induced chemokine cascade promotes breast cancer metastasis by enhancing retention of metastasis-associated macrophages. J ... 2d). CCL2 together with CCL5 were shown to play an important role in breast malignancy and to mediate many types of tumor- ... d 48 h pretreatment of MSC with 1 μg/ml cisplatin increased the level of CXCL1, IL-6, IL-8, CCL2 and MIF cytokines released ...
M-sec regulates polarized secretion of inflammatory endothelial chemokines and facilitates CCL2-mediated lymphocyte ... Tiwari N, Marudamuthu AS, Tsukasaki Y, Ikebe M, Fu J, Shetty S. p53- and PAI-1-mediated induction of C-X-C chemokines and CXCR2 ... Tiwari N, Marudamuthu AS, Puthusseri B, Idell S, Shetty S p53- and PAI-1-mediated induction of C-X-C chemokines and CXCR2: ...
ABBREVIATIONS: ADE: antibody-dependent enhancement; CCL2: monocyte chemoattractant protein-1; CCL3: macrophage inflammatory ... protein-1 α; CCL5: chemokine (C-C motif) ligand 5; CHIKV: chikungunya virus; DCL: diffuse cutaneous leishmaniasis; DENV: dengue ...
... inflammatory chemokines, and apoptosis in the retina of a mouse model of Alzheimer disease (AD). Retinas of transgenic mice ... inflammatory chemokines, and apoptosis in the retina of a mouse model of Alzheimer disease (AD). Retinas of transgenic mice ...
While interferon (IFN)-γ, IL- 12, tumor necrosis factor (TNF)-α, IL-18, transforming growth factor -β and CCL2 have protective ... bone marrow derived or primary cells demonstrate that Salmonella can trigger the synthesis of cytokines and chemokines in ...
CCL2 associated with CD38 expression during ex vivo expansion in human cord blood-derived hematopoietic stem cells. Yao, C. L. ...
  • By in vitro and in vivo migration assays, we show that although CST itself is weakly chemotactic, it blocks migration of monocytes and granulocytes to inflammatory attracting factor CC-chemokine ligand 2 (CCL2) and macrophage inflammatory protein 2 (MIP-2). (biorxiv.org)
  • We reported an association between intrathecal upregulation of C-C chemokine ligand 2(CCL2) and disease severity in ALS. (kyushu-u.ac.jp)
  • Results revealed no significant increase of proinflammatory cytokine/chemokine expressions. (cdc.gov)
  • We analyze the effect of aging on gene expression and chemokine and cytokine networks and show an overall decreased expression of inflammatory mediators together with an increased expression of senescent cells recognition receptors. (elifesciences.org)
  • and notably high expression of a set of chemokines that would favour neutrophil and monocyte recruitment including CXCL2, CCL2, CXCL12, CXCL1, CXCL6, CCL28. (garvan.org.au)
  • Human Qbeads Inflammation Panel Kit allows the measurement of seven human cytokines and chemokines from either serum or in vitro samples. (sartorius.com)
  • The integration of pathogen-associated molecular patterns (PAMPs) from microorganisms with their surface receptors in the immune cells, induces the production of several cytokines and chemokines that presents either a pro- and/or anti-inflammatory role by stimulating the secretion of a great variety of antibody subtypes and the activation of mechanisms of controlling the disease, such as the regulatory T cells. (bvsalud.org)
  • Ryo Yamasaki, Wataru Shiraishi, Yu Hashimoto, Senri Kou, Noriko Isobe, C-C chemokine receptor 2+ macrophages in nerves ameliorate motor neuron disease model mice, 63rd Annual meeting of the Japanese Society of Neurology, 2022.04, [Objective]Macrophages expressing C-C chemokine receptor type (2 CCR2)infiltrate into the neural tissues of amyotrophic lateral sclerosis(ALS)patients. (kyushu-u.ac.jp)
  • Here, we report that CST blocks leukocyte migration towards inflammatory chemokines. (biorxiv.org)
  • To compare the temporal and spatial expression patterns of amyloid precursor protein (APP), amyloid-beta deposits, inflammatory chemokines, and apoptosis in the retina of a mouse model of Alzheimer disease (AD). (cngb.org)
  • Chemokine MCP1/CCL2 gene polymorphism influences Henoch-Schönlein purpura susceptibility in Iranian Azeri-Turkish patients. (cdc.gov)
  • Chemokine MCP1/CCL2 and RANTES/CCL5 gene polymorphisms influence Henoch-Schönlein purpura susceptibility and severity. (cdc.gov)
  • Analytes offered in the Human Qbeads Inflammation Panel Kit include: Human Interferon gamma (IFNγ), Interleukin-2 (IL-2), Interleukin-6 (IL-6), CCL2 (MCP-1), CCL3 (MIP-1α), CXCL9 (MIG), and CXCL10 (IP-10). (sartorius.com)
  • The mRNA levels of CCL2, C1ra, C1s, IL-18, IL-1β, TNFα, IL-33 and glial fibrillary acidic protein (GFAP) were significantly increased at day 1 post-RD, reduced gradually and, with the exception of GFAP and C1ra, returned to the basal levels by day 28 in WT mice. (biomedcentral.com)
  • Further, PACE ® treatment significantly decreased neutrophil and macrophage (white blood cell) infiltration into the wound, attenuating both CC- and CXC-chemokines at the wound margin. (sanuwave.com)
  • Surprisingly, Müller cells from IL-33 −/− mice expressed significantly lower levels of CCL2 and IL-6 compared with those from WT mice, particularly under hypoxic conditions, whereas IL-33 −/− bone marrow-derived macrophages expressed higher levels of inducible nitric oxide synthase, TNFα, IL-1β and CCL2 after LPS + IFNγ stimulation compared to WT macrophages. (biomedcentral.com)
  • Serum levels of CCL2 peaked twice during the immune response, once during the early, acute phase and again during the late, chronic phase. (elsevier.com)
  • Interplay between several molecules (cytokines, chemokines, proteases, and inflammatory mediators) culminates in causing damage to the articular cartilage and bones. (hindawi.com)
  • 2016. Voluntary exercise blocks Western diet-induced gene expression of the chemokines CXCL10 and CCL2 in the prefrontal cortex. (uc.edu)
  • In CSF, in patients without central nervous system (CNS) disease/infection, cytokines/chemokines are either undetectable (e.g., interleukin-6 [IL-6], CXCL8/IL-8, CXCL10/IP-10, CXCL9/MIG) or present at low levels (e.g. (cdc.gov)
  • To further elucidate the role of this chemokine in the anti-filarial immune response, we compared CCL2 deficient (CCL2 -/- ) mice to wild-type mice. (elsevier.com)
  • Barzilai S, Blecher-Gonen R, Barnett-Itzhaki Z, Zauberman A, Lebel-Haziv Y, Amit I, Alon R. M-sec regulates polarized secretion of inflammatory endothelial chemokines and facilitates CCL2-mediated lymphocyte transendothelial migration. (famri.org)
  • In IL-33 −/− mice, RD induced an exacerbated inflammatory response with significantly higher levels of CCL2, IL-1β and GFAP when compared to WT. (biomedcentral.com)
  • We observed that CCL2 was expressed by peritoneal exudate cells and was present in the sera of wild-type mice. (elsevier.com)
  • The cytokines/chemokines included are implicated in inflammatory responses to disease states including autoimmune diseases, chronic inflammation, and infections, including viral infections such as COVID-19. (sartorius.com)
  • These NF- kappaB activated islets not only expressed the same chemokine profile observed in human islets, but also struggled to maintain normoglycemia post transplantation. (garvan.org.au)
  • Chemokine gene polymorphisms associate with gender in patients with uveitis. (cdc.gov)
  • Association of ACE, VEGF and CCL2 gene polymorphisms with Henoch-Schönlein purpura and an evaluation of the possible interaction effects of these loci in HSP patients. (cdc.gov)
  • Another reported that IL-10, C-X-C motif chemokine ligand 10 (CXCL-10, formerly IFN-γ inducible protein 10) and CC chemokine ligand 2 (CCL2, formerly monocyte chemoattractant protein 1) levels were higher in patients with high viral loads ( 12 ), but patients with severe disease had higher levels of CXCL10 and CCL2 than did patients with less-severe cases. (cdc.gov)
  • This proposal will test the novel hypothesis that when L. reuteri are decreased due to stressor exposure, colonic epithelial cells overproduce chemokines (particularly CCL2) that increase the recruitment of inflammatory macrophages to the colon where they ultimately exacerbate colitis. (nih.gov)
  • The first aim will examine the role of CCL2 as a novel primary mechanism (pathway) mediating the effects of stress on colonic inflammation, by assessing the effects of stress-induced alterations of L. reuteri on CCL2 production by colonic epithelial cells and by using CCL2 knockout mice. (nih.gov)
  • Finally, in the third aim, we will determine whether the ability of L. reuteri to affect chemokine production by colonic epithelial cells is dependent upon L. reuteri colonizing the colon, and/or due to the production of immunomodulatory factor(s). (nih.gov)
  • Interferon pathway-related cytokines/chemokines, including interleukin (IL) 18, macrophage inflammatory protein 3α, and IL-33, were elevated, but tumor necrosis factor-α, IL-6, CXCL8 (formerly IL-8), and cytokines acting through C-C chemokine receptor 2 and CCR5 were lower among case-patients than controls. (cdc.gov)
  • In addition to their primary role in mediating neuroinflammation, neuroimmune factors, such as cytokines, chemokines, and MHC, are essential for a variety of normal brain functions. (nih.gov)
  • CCL2), cytokines (e.g. (nih.gov)
  • The discussed chemokines in this review, their synonyms, receptors, activities and sources were summarized in Table 4 . (medscape.com)
  • CCL3 in Cancers Chemokine receptors are expressed on APCs and are promising targets for idiotype (Id) vaccines, the V antigenic determinants region produced by B lymphomas and multiple myelomas. (medscape.com)
  • Chemokines are a superfamily of secreted proteins involved in immunoregulatory and inflammatory processes. (nih.gov)
  • In next part of the review, various chemokines with their specific role in altering immune response to combat various diseases especially cancers will be discussed. (medscape.com)
  • [ 116 ] The role of CCL2 in tumor-development and progression is controversial. (medscape.com)
  • C(C)Learing the Role of Chemokines in Pulmonary Fibrosis. (nih.gov)
  • Thus, modulation of EAE with C-C chemokine DNA vaccines is determined by targeting chemokines that are highly transcribed at the site of inflammation at the onset of disease. (medscape.com)
  • LIF, CCL2 and IL-1alpha and the brain inflammation. (cdc.gov)
  • A chemokine that is a chemoattractant for MONOCYTES and may also cause cellular activation of specific functions related to host defense. (nih.gov)
  • Results revealed no significant increase of proinflammatory cytokine/chemokine expressions. (cdc.gov)
  • Upon oral challenge with the murine colonic pathogen Citrobacter rodentium, which induces colonic histopathology with similarities to human IBD, mice exposed to SDR (and thus having lower levels of L. reuteri) had a significant increase in pathogen-induced colitis as indicated by a significant increase in colonic histopathology, chemokines (e.g. (nih.gov)
  • By contrast to above studies, expression of exogenous CCL2 by adenocarcinoma cells augmented the metastatic potential by modulating tumor-associated angiogenesis. (medscape.com)
  • We examined cytokine/chemokine profiles of 9/12 case-patients compared with healthy controls at 3 time intervals. (cdc.gov)