Dictionaries, MedicalClonal Anergy: Functional inactivation of T- or B-lymphocytes rendering them incapable of eliciting an immune response to antigen. This occurs through different mechanisms in the two kinds of lymphocytes and can contribute to SELF TOLERANCE.Dictionaries as Topic: Lists of words, usually in alphabetical order, giving information about form, pronunciation, etymology, grammar, and meaning.HLA-DR7 Antigen: A HLA-DR antigen that is associated with HLA-DRB1 CHAINS encoded by DRB1*07 alleles.Immune Tolerance: 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.Dictionaries, ChemicalT-Lymphocytes: 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.Clone Cells: A group of genetically identical cells all descended from a single common ancestral cell by mitosis in eukaryotes or by binary fission in prokaryotes. Clone cells also include populations of recombinant DNA molecules all carrying the same inserted sequence. (From King & Stansfield, Dictionary of Genetics, 4th ed)Receptors, Antigen, T-Cell: Molecules on the surface of T-lymphocytes that recognize and combine with antigens. The receptors are non-covalently associated with a complex of several polypeptides collectively called CD3 antigens (ANTIGENS, CD3). Recognition of foreign antigen and the major histocompatibility complex is accomplished by a single heterodimeric antigen-receptor structure, composed of either alpha-beta (RECEPTORS, ANTIGEN, T-CELL, ALPHA-BETA) or gamma-delta (RECEPTORS, ANTIGEN, T-CELL, GAMMA-DELTA) chains.Lymphocyte Activation: 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.Signal Transduction: 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.ZAP-70 Protein-Tyrosine Kinase: A protein tyrosine kinase that is required for T-CELL development and T-CELL ANTIGEN RECEPTOR function.Phosphorylation: The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.Receptors, Antigen, B-Cell: IMMUNOGLOBULINS on the surface of B-LYMPHOCYTES. Their MESSENGER RNA contains an EXON with a membrane spanning sequence, producing immunoglobulins in the form of type I transmembrane proteins as opposed to secreted immunoglobulins (ANTIBODIES) which do not contain the membrane spanning segment.Antigens, CD3: Complex of at least five membrane-bound polypeptides in mature T-lymphocytes that are non-covalently associated with one another and with the T-cell receptor (RECEPTORS, ANTIGEN, T-CELL). The CD3 complex includes the gamma, delta, epsilon, zeta, and eta chains (subunits). When antigen binds to the T-cell receptor, the CD3 complex transduces the activating signals to the cytoplasm of the T-cell. The CD3 gamma and delta chains (subunits) are separate from and not related to the gamma/delta chains of the T-cell receptor (RECEPTORS, ANTIGEN, T-CELL, GAMMA-DELTA).Antibodies, Monoclonal: Antibodies produced by a single clone of cells.Fas Ligand Protein: A transmembrane protein belonging to the tumor necrosis factor superfamily that was originally discovered on cells of the lymphoid-myeloid lineage, including activated T-LYMPHOCYTES and NATURAL KILLER CELLS. It plays an important role in immune homeostasis and cell-mediated toxicity by binding to the FAS RECEPTOR and triggering APOPTOSIS.Myasthenia Gravis: A disorder of neuromuscular transmission characterized by weakness of cranial and skeletal muscles. Autoantibodies directed against acetylcholine receptors damage the motor endplate portion of the NEUROMUSCULAR JUNCTION, impairing the transmission of impulses to skeletal muscles. Clinical manifestations may include diplopia, ptosis, and weakness of facial, bulbar, respiratory, and proximal limb muscles. The disease may remain limited to the ocular muscles. THYMOMA is commonly associated with this condition. (Adams et al., Principles of Neurology, 6th ed, p1459)Antigens, CD95: A tumor necrosis factor receptor subtype found in a variety of tissues and on activated LYMPHOCYTES. It has specificity for FAS LIGAND and plays a role in regulation of peripheral immune responses and APOPTOSIS. Multiple isoforms of the protein exist due to multiple ALTERNATIVE SPLICING. The activated receptor signals via a conserved death domain that associates with specific TNF RECEPTOR-ASSOCIATED FACTORS in the CYTOPLASM.Myasthenia Gravis, Autoimmune, Experimental: Any autoimmune animal disease model used in the study of MYASTHENIA GRAVIS. Injection with purified neuromuscular junction acetylcholine receptor (AChR) (see RECEPTORS, CHOLINERGIC) components results in a myasthenic syndrome that has acute and chronic phases. The motor endplate pathology, loss of acetylcholine receptors, presence of circulating anti-AChR antibodies, and electrophysiologic changes make this condition virtually identical to human myasthenia gravis. Passive transfer of AChR antibodies or lymphocytes from afflicted animals to normals induces passive transfer experimental autoimmune myasthenia gravis. (From Joynt, Clinical Neurology, 1997, Ch 54, p3)Membrane Glycoproteins: Glycoproteins found on the membrane or surface of cells.Receptors, Cholinergic: Cell surface proteins that bind acetylcholine with high affinity and trigger intracellular changes influencing the behavior of cells. Cholinergic receptors are divided into two major classes, muscarinic and nicotinic, based originally on their affinity for nicotine and muscarine. Each group is further subdivided based on pharmacology, location, mode of action, and/or molecular biology.Apoptosis: 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.Torpedo: A genus of the Torpedinidae family consisting of several species. Members of this family have powerful electric organs and are commonly called electric rays.Hylobatidae: A family of the suborder HAPLORHINI comprising only one genus, HYLOBATES (also called Nomascus or Symphalangus).BooksPsychology, Comparative: The branch of psychology concerned with similarities or differences in the behavior of different animal species or of different races or peoples.Ficoll: A sucrose polymer of high molecular weight.Perceptual Distortion: Lack of correspondence between the way a stimulus is commonly perceived and the way an individual perceives it under given conditions.Self Concept: A person's view of himself.Recognition (Psychology): The knowledge or perception that someone or something present has been previously encountered.Allied Health Occupations: Occupations of medical personnel who are not physicians, and are qualified by special training and, frequently, by licensure to work in supporting roles in the health care field. These occupations include, but are not limited to, medical technology, physical therapy, physician assistant, etc.Face: The anterior portion of the head that includes the skin, muscles, and structures of the forehead, eyes, nose, mouth, cheeks, and jaw.Radiation Chimera: An organism whose body contains cell populations of different genotypes as a result of the TRANSPLANTATION of donor cells after sufficient ionizing radiation to destroy the mature recipient's cells which would otherwise reject the donor cells.Gastroenterology: A subspecialty of internal medicine concerned with the study of the physiology and diseases of the digestive system and related structures (esophagus, liver, gallbladder, and pancreas).Pediatrics: A medical specialty concerned with maintaining health and providing medical care to children from birth to adolescence.Spleen: An encapsulated lymphatic organ through which venous blood filters.Celiac Disease: A malabsorption syndrome that is precipitated by the ingestion of foods containing GLUTEN, such as wheat, rye, and barley. It is characterized by INFLAMMATION of the SMALL INTESTINE, loss of MICROVILLI structure, failed INTESTINAL ABSORPTION, and MALNUTRITION.Ovalbumin: An albumin obtained from the white of eggs. It is a member of the serpin superfamily.Autoimmune Diseases: Disorders that are characterized by the production of antibodies that react with host tissues or immune effector cells that are autoreactive to endogenous peptides.Antigens: Substances that are recognized by the immune system and induce an immune reaction.Administration, Oral: The giving of drugs, chemicals, or other substances by mouth.Drug Tolerance: Progressive diminution of the susceptibility of a human or animal to the effects of a drug, resulting from its continued administration. It should be differentiated from DRUG RESISTANCE wherein an organism, disease, or tissue fails to respond to the intended effectiveness of a chemical or drug. It should also be differentiated from MAXIMUM TOLERATED DOSE and NO-OBSERVED-ADVERSE-EFFECT LEVEL.Norovirus: A genus in the family CALICIVIRIDAE, associated with epidemic GASTROENTERITIS in humans. The type species, NORWALK VIRUS, contains multiple strains.Caliciviridae Infections: Virus diseases caused by CALICIVIRIDAE. They include HEPATITIS E; VESICULAR EXANTHEMA OF SWINE; acute respiratory infections in felines, rabbit hemorrhagic disease, and some cases of gastroenteritis in humans.Virus Inactivation: Inactivation of viruses by non-immune related techniques. They include extremes of pH, HEAT treatment, ultraviolet radiation, IONIZING RADIATION; DESICCATION; ANTISEPTICS; DISINFECTANTS; organic solvents, and DETERGENTS.Virus Replication: 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.Immunologic Memory: The altered state of immunologic responsiveness resulting from initial contact with antigen, which enables the individual to produce antibodies more rapidly and in greater quantity in response to secondary antigenic stimulus.Orthomyxoviridae Infections: Virus diseases caused by the ORTHOMYXOVIRIDAE.Mice, Inbred C57BLAntibodies, Viral: Immunoglobulins produced in response to VIRAL ANTIGENS.Carbocysteine: A compound formed when iodoacetic acid reacts with sulfhydryl groups in proteins. It has been used as an anti-infective nasal spray with mucolytic and expectorant action.Cell Line: Established cell cultures that have the potential to propagate indefinitely.Hygiene Hypothesis: The theory that infectious agents, symbiotic microorganisms, and parasites are normal stimulants for the maturation of the immune system toward a balanced immune response. The theory predicts that lack of such stimulation leads to allergies and AUTOIMMUNE DISEASES.Encyclopedias as Topic: Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)Communicable DiseasesHygiene: The science dealing with the establishment and maintenance of health in the individual and the group. It includes the conditions and practices conducive to health. (Webster, 3d ed)Autoimmunity: Process whereby the immune system reacts against the body's own tissues. Autoimmunity may produce or be caused by AUTOIMMUNE DISEASES.Communicable Diseases, Emerging: Infectious diseases that are novel in their outbreak ranges (geographic and host) or transmission mode.MedlinePlus: NATIONAL LIBRARY OF MEDICINE service for health professionals and consumers. It links extensive information from the National Institutes of Health and other reviewed sources of information on specific diseases and conditions.Molecular Sequence Data: 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.Communicable Disease Control: Programs of surveillance designed to prevent the transmission of disease by any means from person to person or from animal to man.Vitiligo: A disorder consisting of areas of macular depigmentation, commonly on extensor aspects of extremities, on the face or neck, and in skin folds. Age of onset is often in young adulthood and the condition tends to progress gradually with lesions enlarging and extending until a quiescent state is reached.Faculty, Medical: The teaching staff and members of the administrative staff having academic rank in a medical school.MassachusettsDermatology: A medical specialty concerned with the skin, its structure, functions, diseases, and treatment.Schools, Medical: Educational institutions for individuals specializing in the field of medicine.Rats, Inbred BB: A strain of Rattus norvegicus which is a model for spontaneous insulin-dependent diabetes mellitus (DIABETES MELLITUS, INSULIN-DEPENDENT).History, 20th Century: Time period from 1901 through 2000 of the common era.Schools: Educational institutions.Hypericum: Genus of perennial plants in the family CLUSIACEAE (sometimes classified as Hypericaceae). Herbal and homeopathic preparations are used for depression, neuralgias, and a variety of other conditions. Hypericum contains flavonoids; GLYCOSIDES; mucilage, TANNINS; volatile oils (OILS, ESSENTIAL), hypericin and hyperforin.Education, Medical: Use for general articles concerning medical education.

Immune surveillance against a solid tumor fails because of immunological ignorance. (1/699)

Many peripheral solid tumors such as sarcomas and carcinomas express tumor-specific antigens that can serve as targets for immune effector T cells. Nevertheless, overall immune surveillance against such tumors seems relatively inefficient. We studied immune surveillance against a s.c. sarcoma expressing a characterized viral tumor antigen. Surprisingly, the tumor cells were capable of inducing a protective cytotoxic T cell response if transferred as a single-cell suspension. However, if they were transplanted as small tumor pieces, tumors readily grew. Tumor growth correlated strictly with (i) failure of tumor cells to reach the draining lymph nodes and (ii) absence of primed cytotoxic T cells. Cytotoxic T cells were not tolerant or deleted because a tumor antigen-specific cytotoxic T cell response was readily induced in lymphoid tissue by immunization with virus or with tumor cells even in the presence of large tumors. Established tumors were rejected by vaccine-induced effector T cells if effector T cells were maintained by prolonged or repetitive vaccination, but not by single-dose vaccination. Thus, in addition to several other tumor-promoting parameters, some antigenic peripheral sarcomas-and probably carcinomas-may grow not because they anergize or tolerize tumor-specific T cells, but because such tumors are immunologically dealt with as if they were in a so-called immunologically privileged site and are ignored for too long.  (+info)

Inhibition of cell cycle progression by rapamycin induces T cell clonal anergy even in the presence of costimulation. (2/699)

Costimulation (signal 2) has been proposed to inhibit the induction of T cell clonal anergy by either directly antagonizing negative signals arising from TCR engagement (signal 1) or by synergizing with signal 1 to produce IL-2, which in turn leads to proliferation and dilution of negative regulatory factors. To better define the cellular events that lead to the induction of anergy, we used the immunosuppressive agent rapamycin, which blocks T cell proliferation in late G1 phase but does not affect costimulation-dependent IL-2 production. Our data demonstrate that full T cell activation (signal 1 plus 2) in the presence of rapamycin results in profound T cell anergy, despite the fact that these cells produce copious amounts of IL-2. Similar to conventional anergy (induction by signal 1 alone), the rapamycin-induced anergic cells show a decrease in mitogen-activated protein kinase activation, and these cells can be rescued by culture in IL-2. Interestingly, the rapamycin-induced anergic cells display a more profound block in IL-3 and IFN-gamma production upon rechallenge. Finally, in contrast to rapamycin, full T cell activation in the presence of hydroxyurea (which inhibits the cell cycle in early S phase) did not result in anergy. These data suggest that it is neither the direct effect of costimulation nor the subsequent T cell proliferation that prevents anergy induction, but rather the biochemical events that occur upon progression through the cell cycle from G1 into S phase.  (+info)

IL-10-induced anergy in peripheral T cell and reactivation by microenvironmental cytokines: two key steps in specific immunotherapy. (3/699)

Specific immunotherapy (SIT) is widely used for treatment of allergic diseases and could potentially be applied in other immunological disorders. Induction of specific unresponsiveness (anergy) in peripheral T cells and recovery by cytokines from the tissue microenvironment represent two key steps in SIT with whole allergen or antigenic T cell peptides (PIT). The anergy is directed against the T cell epitopes of the respective antigen and characterized by suppressed proliferative and cytokine responses. It is initiated by autocrine action of IL-10, which is increasingly produced by the antigen-specific T cells. Later in therapy, B cells and monocytes also produce IL-10. The anergic T cells can be reactivated by different cytokines. Whereas IL-15 and IL-2 generate Th1 cytokine profile and an IgG4 antibody response, IL-4 reactivates a Th2 cytokine pattern and IgE antibodies. Increased IL-10 suppresses IgE and enhances IgG4 synthesis, resulting in a decreased antigen-specific IgE:IgG4 ratio, as observed normally in patients after SIT or PIT. The same state of anergy against the major bee venom allergen, phospholipase A2, can be observed in subjects naturally anergized after multiple bee stings. Together, these data demonstrate the pivotal role of autocrine IL-10 in induction of specific T cell anergy and the important participation of the cytokine microenvironment in SIT. Furthermore, knowledge of the mechanisms explaining reasons for success or failure of SIT may enable possible predictive measures of the treatment.  (+info)

A logical analysis of T cell activation and anergy. (4/699)

Interaction of the antigen-specific receptor of T lymphocytes with its antigenic ligand can lead either to cell activation or to a state of profound unresponsiveness (anergy). Although subtle changes in the nature of the ligand or of the antigen-presenting cell have been shown to affect the outcome of T cell receptor ligation, the mechanism by which the same receptor can induce alternative cellular responses is not completely understood. A model for explaining both positive (cell proliferation and cytokine production) and negative (anergy induction) signaling of T lymphocytes is described herein. This model relies on the autophosphorylative properties of the tyrosine kinases associated with the T cell receptor. One of its basic assumptions is that the kinase activity of these receptor-associated enzymes remains above background level after ligand removal and is responsible for cellular unresponsiveness. Using a simple Boolean formalism, we show how the timing of the binding and intracellular signal-transduction events can affect the properties of receptor signaling and determine the type of cellular response. The present approach integrates into a common framework a large body of experimental observations and allows specification of conditions leading to cellular activation or to anergy.  (+info)

Golli-induced paralysis: a study in anergy and disease. (5/699)

The Golli-MBP transcription unit contains three Golli-specific exons as well as the seven exons of the classical myelin basic protein (MBP) gene and encodes alternatively spliced proteins that share amino acid sequence with MBP. Unlike MBP, which is a late Ag expressed only in the nervous system, Golli exon-containing gene products are expressed both pre- and postnatally at many sites, including lymphoid tissue, as well as in the central nervous system. To investigate whether Golli-MBP peptides unique to Golli would result in neurological disease, we immunized rats and observed a novel neurological disease characterized by mild paralysis and the presence of groups of lymphocytes in the subarachnoid space but not in the parenchyma of the brain. Disease was induced by Th1-type T cells that displayed an unusual activation phenotype. Primary stimulation in vitro induced T cell proliferation with increased surface CD45RC that did not become down-regulated as it did in other Ag-stimulated cultures. Secondary stimulation of this CD45RChigh population with Ag, however, did not induce proliferation or IL-2 production, although an IFN-gamma-producing population resulted. Proliferation could be induced by secondary stimulation with IL-2 or PMA-ionomycin, suggesting an anergic T cell population. Cells could adoptively transfer disease after secondary stimulation with IL-2, but not with Ag alone. These responses are suggestive of a chronically stimulated, anergic population that can be transiently activated to cause disease, fall back into an anergic state, and reactivated to cause disease again. Such a scenario may be important in chronic human disease.  (+info)

Two mechanisms for the non-MHC-linked resistance to spontaneous autoimmunity. (6/699)

Genetic susceptibility and resistance to most autoimmune disorders are associated with highly polymorphic genes of the MHC and with non-MHC-linked polygenic modifiers. It is known that non-MHC-linked polymorphisms can override or enhance the susceptibility to an autoimmune disease provided by pathogenic MHC genes, but the mechanisms remain elusive. In this study, we have followed the fate of two highly diabetogenic beta cell-specific T cell receptors (Kd and I-Ag7 restricted, respectively) in NOR/Lt mice, which are resistant to autoimmune diabetes despite expressing two copies of the diabetogenic MHC haplotype H-2g7. We show that at least two mechanisms of non-MHC-linked control of pathogenic T cells operate in these mice. One segregates as a recessive trait and is associated with a reduction in the peripheral frequency of diabetogenic CD8+ (but not CD4+) T cells. The other segregates as a dominant trait and is mediated by IL-4- and TGF-beta1-independent immune suppressive functions provided by lymphocytes that target diabetogenic CD4+ and CD8+ T cells, without causing their deletion, anergy, immune deviation, or ignorance. These results provide explanations as to how non-MHC-linked polymorphisms can override the susceptibility to an autoimmune disease provided by pathogenic MHC haplotypes, and demonstrate that protective non-MHC-linked genes may selectively target specific lymphoid cell types in cellularly complex autoimmune responses.  (+info)

Superantigen-induced T cell responses in acute rheumatic fever and chronic rheumatic heart disease patients. (7/699)

CD4+ and CD8+ T cells from healthy donors, acute rheumatic fever (ARF) and chronic rheumatic heart disease (CRHD) patients responded variably to a superantigen from Streptococcus pyogenes--Streptococcal pyrogenic erythrogenic toxin A (SPE-A). In vitro culture of CD4+ T cells from ARF patients (CD4-ARF) with SPE-A exhibited a Th1 type of response as they produced high levels of IL-2, while CD4+ T cells from CRHD patients (CD4-RHD) secreted IL-4 and IL-10 in large amounts, i.e. Th2 type of cytokine profile. The skewing of human CD4+ T cells (in response to SPE-A stimulation) to Th1 or Th2 type reflects the role of the two subsets in a disorder with differing intensities at the two extremes of the spectrum. Moreover, the anergy induction experiments revealed that CD8-ARF and CD8-RHD undergo anergy (to different extents), whereas CD4+ T cells do not, in response to re-stimulation by SPE-A. These results initially demonstrate that both CD4+ and CD8+ T cells respond differentially to SPE-A, and hence it is an important observation with respect to the pathogenesis of ARF/CRHD. Anergy in CD8+ T cells in the presence of SPE-A in vitro goes a step further to show the clinical relevance of these cells and their possible role in suppression of the disease.  (+info)

Thymus and autoimmunity: production of CD25+CD4+ naturally anergic and suppressive T cells as a key function of the thymus in maintaining immunologic self-tolerance. (8/699)

This study shows that the normal thymus produces immunoregulatory CD25+4+8- thymocytes capable of controlling self-reactive T cells. Transfer of thymocyte suspensions depleted of CD25+4+8- thymocytes, which constitute approximately 5% of steroid-resistant mature CD4+8- thymocytes in normal naive mice, produces various autoimmune diseases in syngeneic athymic nude mice. These CD25+4+8- thymocytes are nonproliferative (anergic) to TCR stimulation in vitro, but potently suppress the proliferation of other CD4+8- or CD4-8+ thymocytes; breakage of their anergic state in vitro by high doses of IL-2 or anti-CD28 Ab simultaneously abrogates their suppressive activity; and transfer of such suppression-abrogated thymocyte suspensions produces autoimmune disease in nude mice. These immunoregulatory CD25+4+8- thymocytes/T cells are functionally distinct from activated CD25+4+ T cells derived from CD25-4+ thymocytes/T cells in that the latter scarcely exhibits suppressive activity in vitro, although both CD25+4+ populations express a similar profile of cell surface markers. Furthermore, the CD25+4+8- thymocytes appear to acquire their anergic and suppressive property through the thymic selection process, since TCR transgenic mice develop similar anergic/suppressive CD25+4+8- thymocytes and CD25+4+ T cells that predominantly express TCRs utilizing endogenous alpha-chains, but RAG-2-deficient TCR transgenic mice do not. These results taken together indicate that anergic/suppressive CD25+4+8- thymocytes and peripheral T cells in normal naive mice may constitute a common T cell lineage functionally and developmentally distinct from other T cells, and that production of this unique immunoregulatory T cell population can be another key function of the thymus in maintaining immunologic self-tolerance.  (+info)

*Clonal anergy

Jenkins, Marc K. (February 1992). "The role of cell division in the induction of clonal anergy". Immunology Today. 13 (2): 69- ... Clonal anergy at the US National Library of Medicine Medical Subject Headings (MeSH). ... Strong stimulation of T-cells either by IL-2 or by TCR/costimulatory receptors can break the anergy. Anergy may be taken ... Various chemicals inducing/inhibiting described T cell signalling pathways can be used to study the anergy. The anergy in T ...

*Autoimmunity

Pike B, Boyd A, Nossal G (1982). "Clonal anergy: the universally anergic B lymphocyte". Proceedings of the National Academy of ... Clonal Anergy theory, proposed by Nossal, in which self-reactive T- or B-cells become inactivated in the normal individual and ... In addition, two other theories are under intense investigation: Clonal Ignorance theory, according to which autoreactive T ... Three hypotheses have gained widespread attention among immunologists: Clonal Deletion theory, proposed by Burnet, according to ...

*Molecular mimicry

... is known as clonal anergy. The mechanism of clonal anergy is important to maintain tolerance to many autologous antigens. ... Just as in T cells, clonal deletion and clonal anergy can physically eliminate autoreactive B cell clones. Receptor editing is ... This negative selection is known as clonal deletion, one of the mechanisms for B cell tolerance. Approximately 0.99 percent of ...

*Clonal deletion

T lymphocytes can instead undergo clonal arrest, clonal anergy, and clonal editing. If autoreactive cells escape clonal ... Thus, clonal deletion can help protect individuals against autoimmunity. Clonal deletion is thought to be the most common type ... Incomplete clonal deletion results in apoptosis of most autoreactive B and T lymphocytes. Complete clonal deletion can lead to ... Clonal deletion is the removal through apoptosis of B cells and T cells that have expressed receptors for self before ...

*Clonal

... a model for how the immune system responds to infection Clonal anergy, a lack of reaction by the body's defense mechanisms to ... Clonal may refer to in Immunology Clonal deletion, a process by which B cells and T cells are deactivated before act ... also called clonal anemone Vegetative cloning, a form of asexual reproduction in plants Clone (disambiguation) Clonalis House ... foreign substance in Biology Clonal interference, a phenomenon that occurs when two (or more) beneficial mutations arise ...

*Short course immune induction therapy

... clonal anergy, deletion, and ignorance. While autoimmunity is thought to result from the breakdown of central and peripheral ... Data from follow up studies suggest that anti-CD3 antibody treatment caused not only anergy induction and transient depletion ... and anergy induction. Results from a clinical trial in 2000 showed that treatment with the modified form of anti-CD3 preserved ...

*List of MeSH codes (G04)

... clonal anergy MeSH G04.610.484.120 --- clonal deletion MeSH G04.610.484.800 --- self tolerance MeSH G04.610.484.910 --- ...

*Index of immunology articles

Clonal anergy Clonal deletion Clonal selection Clone (cell biology) CMKLR1 Colony stimulating factor 1 receptor Colony- ...

*Outline of immunology

Self-proteins Autoimmunity Alloimmunity Cross-reactivity Tolerance Central tolerance Peripheral tolerance Clonal anergy Clonal ... Mimotope Tumor antigen Antigen-antibody interaction Immunogenetics Affinity maturation Somatic hypermutation Clonal selection V ...

*Tolerogenic therapy

This can induce T cell clonal deletion, T cell anergy or the proliferation of regulatory T cells (Tregs). Collectively, these ...

*B cell

... clonal deletion, receptor editing, anergy, or ignorance (B cell ignores signal and continues development). This negative ...

*Peripheral tolerance

Mechanisms of peripheral tolerance include direct inactivation of effector T cells by either clonal deletion, conversion to ... and so anergy will result if there is an MHC-TCR interaction between the T cell and the APC. Since many pathways of immunity ... regulatory T cells (Tregs) or induction of anergy. Tregs, which are also generated during thymic T cell development, further ...

*Uveitis

April 2007). "Limited peripheral T cell anergy predisposes to retinal autoimmunity". J. Immunol. 178 (7): 4276-83. doi:10.4049/ ... and cellular stress is normally suppressed by myeloid suppression while inducible Treg cells prevent activation and clonal ... or a state of anergy is induced to prevent self targeting. Autoreactive T cells must normally be held in check by the ...

*Harald von Boehmer

Nature 333, 742-746 (1988); Swat, W., Ignatowicz, L., von Boehmer, H. and Kisielow, P.: Clonal deletion of immature CD4+8+ ... Science 251, 1225 (1991). Peripheral tolerance by deletion of and reversible anergy in matureT cells. Borgulya, P., Kishi, H., ...

*Immunosuppressive drug

By preventing the clonal expansion of lymphocytes in the induction phase of the immune response, it affects both the cell and ... The cross-binding of CD3 molecules as well activates an intracellular signal causing the T cell anergy or apoptosis, unless the ... preventing the IL-2 induced clonal expansion of activated lymphocytes and shortening their survival. They are used in the ... namely signal transduction and lymphocyte clonal proliferation. It binds to FKBP1A like tacrolimus, however the complex does ...

*T helper cell

This results in the cell becoming anergic (anergy is generated from the unprotected biochemical changes of Signal 1). Anergic ... secretion of IL-2 can bind to that same Th cell or neighboring Th's via the IL-2R thus driving proliferation and clonal ...

*Influenza treatment

Clonal populations of CD8+ cytotoxic T cells have been grown which carry T cell receptors specific to influenza. These work ... The authors concluded that resistance to flu symptoms was associated with a shift in cell mediated immunity from anergy toward ...

*Ipilimumab

Kearney E.R.; Walunas T.L.; Karr R.W.; Morton P.A.; Loh D.Y.; Bluestone J.A.; Jenkins M.K. (1995). "Antigen-dependent clonal ... "CD28 mediated signalling costimulates murine T cells and prevents the induction of anergy in T cell clones". Nature. 356 (6370 ...

*T cell

Virtual memory T cells differ from the other memory subsets in that they do not originate following a strong clonal expansion ... T cell receptor signalling alone results in anergy. The signalling pathways downstream from co-stimulatory molecules usually ... Increasing evidence indicates microRNAs, which are small noncoding regulatory RNAs, could impact the clonal selection process ...

*Immune tolerance

DCs also have the capacity to directly induce anergy in T cells that recognize antigen expressed at high levels and thus ... now termed clonal deletion. Burnet and Medawar were ultimately credited for "the discovery of acquired immune tolerance" and ... inducing anergy (reduced proliferation and IL-2 signaling) Interaction with B7 on T cells Downregulation of CD80/CD86 ... or by induction of anergy, a state of non-activity. Weakly autoreactive B cells may also remain in a state of immunological ...

*Adaptive immune system

Myriad receptors are produced through a process known as clonal selection. According to the clonal selection theory, at birth, ... Affinity maturation Allelic exclusion Anergy Immune tolerance Immunosuppression Original antigenic sin Somatic hypermutation ... This theory, which builds on established concepts of clonal selection, is being applied in the search for an HIV vaccine. ... Once activated, the CTL undergoes a process called clonal selection, in which it gains functions and divides rapidly to produce ...
Anergy is a term in immunobiology that describes a lack of reaction by the bodys defense mechanisms to foreign substances, and consists of a direct induction of peripheral lymphocyte tolerance. An individual in a state of anergy often indicates that the immune system is unable to mount a normal immune response against a specific antigen, usually a self-antigen. Lymphocytes are said to be anergic when they fail to respond to their specific antigen. Anergy is one of three processes that induce tolerance, modifying the immune system to prevent self-destruction (the others being clonal deletion and immunoregulation). This phenomenon was first described in B lymphocytes by Gustav Nossal and termed "clonal anergy." The clones of B lymphocytes in this case can still be found alive in the circulation, but are ineffective at mounting immune responses. Later Ronald Schwartz and Marc Jenkins described a similar process operating in the T lymphocyte. Many viruses (HIV being the most extreme example) seem ...
Tcell anergy is one of the mechanisms thought to act in the periphery to ensure tolerance to self. The term anergy was first used to describe T cell clones rendered unresponsive to subsequent restimulation by first activating them through the TCR (signal 1) without appropriate costimulation (signal 2) (1) or, more recently, using an altered peptide ligand for activation (2). The characteristic feature of this induced unresponsiveness was the inability of the anergic T cells to proliferate or produce IL-2 following subsequent optimal restimulation (3). Anergic T cells appeared to have a defect in signaling pathways upstream of transcription of the IL-2 gene (4, 5, 6). Additional studies demonstrated the presence of cis-dominant negative regulatory elements affecting IL-2 transcription (7, 8). The recent finding of increased general receptor of phosphoinositides-1 expression indicated that broader genetic changes may accompany the induction and maintenance of the anergic phenotype (9). Our ...
It has been observed that coincident with or immediately following IκBα degradation, p65 is phosphorylated at multiple residues, and these phosphorylation events are necessary for proper regulation of NF-κB function (45). The phosphorylation patterns of NF-κB proteins have not been characterized in T cell anergy, and so we asked whether aberrant phosphorylation was responsible for the defects in NF-κB function in anergic cells. An early step involves phosphorylation of p65 at Ser536 by the IKK complex (32-35), and it has been suggested that phosphorylation at this residue negatively regulates the kinetics of p65 nuclear translocation (33). We found that p65 is phosphorylated at Ser536 equivalently in both naive and anergic cells, which is consistent with our finding that p65 translocates to the nucleus with normal kinetics in anergic T cells. A second posttranslational modification important for NF-κB activity is phosphorylation at Ser276. We found that, as with Ser536 phosphorylation, p65 ...
Induction and maintenance of unresponsiveness of B cells that recognize low valency autoantigens presents a challenging biological problem. Such antigens, even if they have high affinity for the BCR, are likely to induce relative weak signals because they do not aggregate receptors efficiently. Available evidence suggests that when autoantigen avidity and, consequently, ability to induce signaling is not sufficient to induce editing or clonal deletion, autoreactive B cells may be rendered anergic. Chronic stimulation by such antigens leads to changes in intracellular signaling circuitry that makes the cell unresponsive to a variety of signals, including aggregation of previously unoccupied BCR. This unresponsiveness is not durable, as would be expected if it were mediated by genetic reprogramming. Removal of autoantigen from BCR can lead to restoration of responsiveness within minutes, suggesting maintenance by activation of labile regulatory signaling pathways (Gauld et al., 2005). Definitive ...
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Looking for online definition of Clonal anergy in the Medical Dictionary? Clonal anergy explanation free. What is Clonal anergy? Meaning of Clonal anergy medical term. What does Clonal anergy mean?
TY - JOUR. T1 - Targeting B-cell anergy in chronic lymphocytic leukemia.. AU - Apollonio, Benedetta. AU - Scielzo, Cristina. AU - Bertilaccio, Maria Teresa Sabrina. AU - Ten Hacken, Elisa. AU - Scarfò, Lydia. AU - Ranghetti, Pamela. AU - Stevenson, Freda. AU - Packham, Graham. AU - Ghia, Paolo. AU - Muzio, Marta. AU - Caligaris-Cappio, Federico. PY - 2013/5/9. Y1 - 2013/5/9. N2 - B-cell receptor (BCR) triggering and responsiveness have a crucial role in the survival and expansion of chronic lymphocytic leukemia (CLL) clones. Analysis of in vitro response of CLL cells to BCR triggering allowed the definition of 2 main subsets of patients and lack of signaling capacity was associated with constitutive activation of extracellular-regulated kinases 1/2 (ERK1/2) and nuclear factor of activated T cells c1 (NF-ATc1), consistent with the idea that at least one group of CLL patients derives from the abnormal expansion of anergic B cells. In the present work, we further investigated the anergic subset of ...
Sustained calcium signaling induces a state of anergy or antigen unresponsiveness in T cells, mediated through calcineurin and the transcription factor NFAT. We show here that Ca(2+)-induced anergy is a multistep program that is implemented at least partly through proteolytic degradation of specific signaling proteins. Calcineurin increased mRNA and protein of the E3 ubiquitin ligases Itch, Cbl-b and GRAIL and induced expression of Tsg101, the ubiquitin-binding component of the ESCRT-1 endosomal sorting complex. Subsequent stimulation or homotypic cell adhesion promoted membrane translocation of Itch and the related protein Nedd4, resulting in degradation of two key signaling proteins, PKC-theta and PLC-gamma1. T cells from Itch- and Cbl-b-deficient mice were resistant to anergy induction. Anergic T cells showed impaired calcium mobilization after TCR triggering and were unable to maintain a mature immunological synapse, instead showing late disorganization of the outer ring containing lymphocyte
In this study, we have shown that bivalent anti-CD3 delivers a partial TCR signal that renders Th1 clones hyporesponsive. This signal consists of phosphorylation of several components of the TCR complex, (bands representing CD3ε, CD3δ), ZAP-70 association, and partial phosphorylation of TCR ζ; in the absence of cross-linking, there is a relatively greater induction of the phosphorylated p21 ζ as compared with the p23 ζ band species evident in T cell clones. Presently, it is unclear what the p21 and p23 forms of ζ represent. p21 induction appears to be sufficient for association of the ZAP-70 kinase with the TCR complex, whereas p23 induction and ZAP-70 phosphorylation appear to be interrelated events. Indeed, the low level of ZAP-70 phosphorylation observed in the noncross-linked situation correlates with the small amount of p23 ζ that is generated. In a recent study, Weist et al. ((28)) proposed that the p23 form of ζ observed in thymocytes upon in vitro stimulation depends on greater ...
Dear Immunonetters, I would like to bring another player into the Self/non-self discrimination arena. That Being the effect of Anergic T-cells on other autoreactive T-cells.This concept has been discussed in the papers by Lasalle and Hafler ( FASEB J. 8:601-608 1994) and Lombardi et al ( science 264:1587 1994). I agree with the authors that the Anergic T-cells play an important rolein self/nonself discrimination. In summary this is whats happening. The Thymus, site of clonal deletion, is very efficient in removing autoreactive T-cells. But nothing is perfect and some autoreactive cells escape this screening. These T-cells can be safely present in the periphery if the antigens they are reactive to are hidden away from them or not presented to them. This is called Clonal Ignorance. If MHC/AG is presented to the autoreactive T-cell but is not followed by costimulation, the result is Clonal anergy. In these cases the T-cells can recognize the self antigen however the extent of the response stops ...
Immunoglobulin superfamily, member 2 (IGSF2) also known as CD101 (Cluster of Differentiation 101), is a human gene. Cluster of differentiation GRCh38: Ensembl release 89: ENSG00000134256 - Ensembl, May 2017 GRCm38: Ensembl release 89: ENSMUSG00000086564 - Ensembl, May 2017 "Human PubMed Reference:". "Mouse PubMed Reference:". "Entrez Gene: IGSF2 immunoglobulin superfamily, member 2". Rivas A, Ruegg CL, Zeitung J, et al. (1995). "V7, a novel leukocyte surface protein that participates in T cell activation. I. Tissue distribution and functional studies". J. Immunol. 154 (9): 4423-33. PMID 7722299. Ruegg CL, Rivas A, Madani ND, et al. (1995). "V7, a novel leukocyte surface protein that participates in T cell activation. II. Molecular cloning and characterization of the V7 gene". J. Immunol. 154 (9): 4434-43. PMID 7722300. Soares LR, Rivas A, Tsavaler L, Engleman EG (1997). "Ligation of the V7 molecule on T cells blocks anergy induction through a CD28-independent mechanism". J. Immunol. 159 (3): ...
1)does costimulatory blockade make the body more prone to illnesses caused by foreign anitigens? since it induces t-cell anergy, or is it specific? because i know that it is used to suppress or prevent some autoimmune/graft effects. 2)i was reading a student report quoted "previous studies have suggested that combined treatment of cytokines may induce immuonological tolerance", however, I cannot find the actual paper, could you please help me out with that? Thankyou and your time and help is greatly appreciated ...
Hepatitis C virus (HCV) is associated with the B-cell lymphoproliferative disorders mixed cryoglobulinemia (MC) and non-Hodgkin lymphoma. We have previously reported that HCV(+)MC(+) patients have clonal expansions of hypermutated, rheumatoid factor-bearing marginal zone-like IgM(+)CD27(+) peripheral B cells using the V(H)1-69 gene. Here we coupled transcriptional profiling with immunophenotypic and functional studies to ascertain these cells role in MC pathogenesis. Despite their fundamental role in MC disease, these B cells have overall transcriptional features of anergy and apoptosis instead of neoplastic transformation. Highly up-regulated genes include SOX5, CD11C, galectin-1, and FGR, similar to a previously described FCRL4(+) memory B-cell subset and to an exhausted, anergic CD21(low) memory B-cell subset in HIV(+) patients. Moreover, HCV(+)MC(+) patients clonal peripheral B cells are enriched with CD21(low), CD11c(+), FCRL4(high), IL-4R(low) memory B cells. In contrast to the functional,
BackgroundHIV specific T cells are putatively anergic in vivo. IL-2, a member of a class of cytokines that binds to receptors containing the common gamma chain (γc) has been shown to reverse anergy. We examined the role of γc cytokines in reversing HIV specific T cell anergy.MethodsPBMC from untreated HIV-infected individuals were briefly exposed to a panel of γc cytokines, and frequencies of gag specific T cells were enumerated by intracellular IFN-γ flow cytometry.ResultsOf the γc cytokines, brief exposure to IL-2, IL-15, or combined IL-15/IL-7 significantly enhanced (range 2-7 fold) the CD4+ and CD8+ T cell IFN-γ responses to HIV gag, with IL-15 giving the greatest enhancement. The effects of cytokines were not due to enhanced proliferation of pre-existing antigen specific cells, but were due to a combination of enhanced cytokine production from antigen specific T cells plus activation of non-epitope specific T cells.ConclusionsThese observations support the notion that a significant number of
In the last 4 years of funding we have defined the conditions under which T cells obviate the requirement for costimulatory signaling during activation, and med...
Update on Staphylococcal Superantigen-Induced Signaling Pathways and Therapeutic Interventions. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
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Mice and in vivo procedures. C57BL/6J mice were bred from mice obtained from The Jackson Laboratory, and Ncr1+/gfp (51) and Ubi-GFP (23) mice were donated by Ofer Mandelboim (Hebrew University, Jerusalem, Israel) and Ellen Robey (University of California, Berkeley, California, USA), respectively. Mice were maintained at the University of California, Berkeley. Sex- and age-matched (6- to 10-week-old) mice were used for the experiments.. Tumor cells resuspended in 100 μl of RPMI without FCS were injected s.c. in the left flank (or in the right flank where indicated). Tumor development and growth were monitored by measurement of the size of the tumors with a caliper.. Where indicated, NK cells were depleted from mice by i.p. injection of 200 μg of PK136 mAb (specific for NKR-P1C, prepared in the laboratory) 5 days after tumor cell injection, repeated weekly for 4 weeks. Where indicated, each mouse received 100 ng of IL-12 (Peprotech) mixed with 100 ng of IL-18 (MBL International Corp.) or 20 μg ...
TY - JOUR. T1 - Fas/fas ligand pathway, apoptosis, and clonal anergy involved in systemic acetylcholine receptor T cell epitope tolerance. AU - Deng, C.. AU - Goluszko, E.. AU - Christadoss, P.. PY - 2001/3/1. Y1 - 2001/3/1. N2 - The cellular mechanisms of high dose systemic acetylcholine receptor (AChR) T cell epitope, α146-162 peptide-induced tolerance in experimental myasthenia gravis were examined. CD4 cells are the prime target for α146-162 peptide-induced tolerance. The expression of CD69, Fas, and B7.2 molecules on AChR-immune lymphocytes was enhanced within 4-12 h after tolerance induction. A high dose of α146-162 peptide in IFA failed to suppress T cell proliferation and/or clinical myasthenia gravis in lpr and gld mice deficient in Fas and Fas ligand, respectively. A high dose of α146-162 peptide in IFA in AChR-immunized mice induced apoptosis of BV6 cells. Further, reconstitution of IL-2 in vitro-recovered α146-162 peptide tolerized T cell proliferation, IFN-γ, and IL-10 ...
Autoantibodies to transglutaminase 2 (TG2) are hallmarks of celiac disease. To address B cell tolerance and autoantibody formation to TG2, we generated immunoglobulin knock-in (Ig KI) mice that express a prototypical celiac patient-derived anti-TG2 B cell receptor equally reactive to human and mouse TG2. We studied B cell development in the presence/absence of autoantigen by crossing the Ig KI mice to Tgm2−/− mice. Autoreactive B cells in Tgm2+/+ mice were indistinguishable from their naive counterparts in Tgm2−/− mice with no signs of clonal deletion, receptor editing, or B cell anergy. The autoreactive B cells appeared ignorant to their antigen, and they produced autoantibodies when provided T cell help. The findings lend credence to a model of celiac disease where gluten-reactive T cells provide help to autoreactive TG2-specific B cells by involvement of gluten-TG2 complexes, and they outline a general mechanism of autoimmunity with autoantibodies being produced by ignorant B cells on ...
Five hundred ninety-two drug users (IDUs) from community settings in San Francisco and Oakland, California, were screened for tuberculosis using the tuberculin skin test, as well as for skin test anergy using two controls: mumps antigen and either tetanus toxoid or Candida. Those nonresponsive to one skin test were more likely to be nonresponsive to another, even after stratifying by HIV status. Skin test anergy (defined as nonresponse to the tuberculin skin test and to both controls) occurred in 37% of HIV-positive and 11% of HIV-negative IDUs (p | O. 001).
In the course of modeling the naturally occurring tumor immunity seen in patients with paraneoplastic cerebellar degeneration (PCD), we discovered an unexpectedly high threshold for breaking CD8+ cytotoxic T cell (CTL) tolerance to the PCD autoantigen, CDR2. While CDR2 expression was previously found to be strictly restricted to immune-privileged cells (cerebellum, testes, and tumors), unexpectedly we have found that T cells also express CDR2. This expression underlies inhibition of CTL activation; CTLs that respond to epithelial cells expressing CDR2 fail to respond to T cells expressing CDR2. This was a general phenomenon, as T cells presenting influenza (flu) antigen also fail to activate otherwise potent flu-specific CTLs either in vitro or in vivo. Moreover, transfer of flu peptide-pulsed T cells into flu-infected mice inhibits endogenous flu-specific CTLs. Our finding that T cells serve as a site of immune privilege, inhibiting effector CTL function, uncovers an autorepressive loop with ...
n-Butyrate derivatives designed to possess G1 blocker activity both in vitro and in vivo were synthesized. The ester (MEB) and ester/amide (BEB) derivatives of butyrate were found to suppress IL-2-stimulated proliferation of Th1 cells in vitro. Unlike MEB and BEB, the amide analog of butyrate, MEBA, did not suppress Th1 cell proliferation in vitro. The lack of activity of MEBA may be related to the slower metabolic hydrolysis of the amide bond in MEBA compared with the ester bond in MEB and BEB. When tested in vivo, both MEB and BEB, but not MEBA, were shown to significantly suppress a primary antibody response to a thymus-dependent antigen. Suppression of antibody production could reflect inhibition of T and/or B cell function. However, subsequent in vivo experiments to more specifically examine the effect of MEB on T cell activity revealed that MEB induced antigen-specific unresponsiveness in CD4+ T cells. The T cell unresponsiveness induced in mice immunized with ovalbumin and treated with ...
Dybul M, Mercier G, Belson M, Hallahan C, Liu S, Perry C, Herpin B, Ehler L, Davey R, Metcalf J, Mican J, Seder R, Fauci AS. CD40 ligand trimer and IL-12 enhance PBMC and CD4+ T-cell proliferation and production of IFN-γ in response to p24 antigen in HIV-infected individuals: potential contribution of anergy in the lack of HIV-specific unresponsiveness. J Immunol. 2000;165:1685-1692 ...
en] Murine AIDS (MAIDS) is caused by infection with the murine leukemia retrovirus RadLV-Rs and is characterized by T-cell anergy and severe immunodeficiency with increased susceptibilty to several experimental opportunistic infections as observed in HIV infection. T cell anergy is associated with an increase of intracellular cAMP level, triggering a multistep pathway involving activation of PKA type I and resulting in inhibition of proximal TCR signaling. We have reviously demonstrated that blocking PKA type I using the selective inhibitor Rp-8-Br-cAMPS, restores T-cell function in vitro in MAIDS as well as in HIV infection. In the present report, we investigated the effect of parenteral administration of Rp-8-Br-cAMPS in mice with MAIDS. We show that the compound is not toxic and partially restores the ex vivo proliferative responses to anti-CD3 mAb, but that it has no effect on the lymphadenopathy and splenomegaly characterizing ...
Transplantation tolerance across histoincompatibilities in multiple non-H-2 minors (B10.BR into CBA/Ca) and minor plus H-2D (B10.A into CBA/Ca) antigens has been achieved successfully by combined adult bone marrow transplantation and treatment with CD4 and CD8 mAbs. The tolerant state was confirmed by permanent acceptance of donor strain skin grafts, and in vitro unresponsiveness to donor cells. Tolerance was associated with partial donor chimerism to various degrees. Tolerance to minor transplantation antigens induced in this manner was restricted to recipient-type MHC. The possibility was raised that tolerance resulted, at least in part, from clonal anergy rather than deletion.
0121] 1. Shortman K, and Caux C. Dendritic cell development: multiple pathways to natures adjuvants Stem Cells 15:409-419, 1997. [0122] 2. Steinbrink K, Graulich E, Kubsch S, Knop J, Enk A H. CD4(+) and CD8(+) anergic T cells induced by interleukin-10-treated human dendritic cells display antigen-specific suppressor activity. Blood 99: 2468-2476, 2002. [0123] 3. Kusuhara M, Matsue K, Edelbaum D, Loftus J, Takashima A, Matsue H. Killing of naive T cells by CD95L-transfected dendritic cells (DC): in vivo study using killer DC-DC hybrids and CD4(+) T cells from DO11.10 mice. Eur J Immunol 32:1035-1043, 2002. [0124] 4. Gunzer M, Janich S, Varga G, Grabbe S. Dendritic cells and tumor immunity. Semin Immunol 13:291-302, 2001. [0125] 5. Luft T, Luetjens P, Hochrein H, Toy T, Masterman K A, Rizkalla M, Maliszewski C, Shortman K, Cebon J, and Maraskovsky E. IFN-alpha enhances CD40 ligand-mediated activation of immature monocyte-derived dendritic cells. Int Immunol 14:367-380, 2002. [0126] 6. Skov S, ...
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To optimize antigen specific immune responses, immunologists have been focusing on strategies based on targeting antigenic determinants to specific receptors expressed by defined subsets of professional antigen presenting cells (pAPCs). For instance, the most efficient delivery systems rely on co-administration of both antigens and adjuvants to activate pAPCs cells such as dendritic cells (DCs) and to improve their efficacy. Co-delivery of both antigen and adjuvant into the same cell allows for only cells which have internalised the antigen to receive the activation signal, avoiding induction of T cell anergy in the absence of co-stimuli and non-specific activation of APCs which have not seen the antigen. pAPCs, like DCs, also regulate innate immune responses through the expression and activation of various pattern recognition receptors (PRR), like Toll-like receptors, NOD-like receptors and cytosolic DNA and/or RNA sensors. Therefore, the most efficient way to mount a sustained immune response is to
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T lymphocytes from sufferers with sarcoidosis respond when stimulated with mitogen or antigen weakly. arousal of NF-κB-deficient sarcoid T cells led to reduced appearance of Compact disc69 and Compact disc154 reduced proliferation and cytokine (i.e. interleukin 2 [IL-2] and gamma interferon [IFN-γ]) Rilpivirine creation. The clinical need for these findings is normally suggested with the association between low p65 amounts and the advancement of more serious and energetic sarcoidosis. Although correlative our outcomes support a model where multiple intrinsic signaling flaws donate to peripheral T-cell anergy as well as the persistence of chronic irritation in sarcoidosis. Sarcoidosis is normally a multisystem disease of unidentified etiology seen as a noncaseating granuloma development (15 32 It really is connected with anergic replies to skin lab tests and despondent peripheral T-lymphocyte replies (16 34 Many studies have analyzed the systems of peripheral anergy in sarcoidosis. Early ...
Organ transplantation is accompanied by nonspecific immune suppression...It was known that anergic T cells (immune T cells that do not respond ...The authors stimulate recipient T cells from the monkeys with donor ce...Title: Renal allograft rejection is prevented by adoptive transfer of ...,Monkeying,around,to,improve,organ,transplantation,biological,biology news articles,biology news today,latest biology news,current biology news,biology newsletters
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For prototype, coverage of topics pertaining to chemical bye-law and risk assessment is reduced; this place, an apology is offered to any readers seeking to extend their knowledge of these vital topics. Spur on activities that goad increment; these activities drive vary from nipper to babe depending on whether the newborn also demonstrates damage in other areas, such as hearing or motor skills. Rigorously talking, glyconutrients do not help or meliorate some of your wounds of diseases by themselves order voveran sr 100 mg on-line back spasms 38 weeks pregnant. The say of antibodies to block T-cell inhibitory receptors such as CTLA-4 and PD-1 can take to incessant activation and proliferation of tumor-specific T cells, preventing anergy or fatigue and thereby allowing the advancement of an effec- tive tumor-specific invulnerable response. Besides the held venture is expected to be filtered alongside notoriety amplification of the stimulus figure so that exclusively a suitably active figurine ...
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Tuberculin skin testing with tuberculin purified protein derivative (PPD) is used to screen persons for latent tuberculosis (TB) infection. However, it is not a perfect screening test, and anergy testing, performed along with PPD, has been proposed as a method of determining a persons ability to exhibit a delayed-type hypersensitivity response, and thus, to "verify" a negative tuberculin skin test result.. By the 1970s, anergy testing was routinely performed when a PPD was performed, despite the lack of data supporting this step. In 1991, the Centers for Disease Control and Prevention (CDC) issued guidelines recommending anergy testing as an adjunct to tuberculin testing when screening persons who were human immunodeficiency virus (HIV)-positive for latent tuberculosis. The CDC later revised these guidelines and withdrew this recommendation. It is known that some persons with TB exhibit specific anergy to tuberculin but still respond to other antigens, possibly because available T-cell ...
The main interest of Dr. Son is to address relevant questions and make significant contributions to the understanding of lupus and autoimmune disease, as well as to the development of effective therapies. In addition, she would like to bring her expertise and enthusiasm to guide young scientists.. Dr. Son pursued her PhD at Ewha Womans University in Seoul, Korea where she carried out studies of T-cell homeostasis as well as peripheral T cell tolerance. Dr. Son identified a novel gene, LIME, and characterized its function in T cells in vitro and in vivo in the lab of Dr. Yungdae Yun of the Division of Life Science.. After receiving her PhD degree, Dr. Son remained in the Dr. Yuns lab to continue her research as a Post-doctoral research fellow. After two years, she was promoted to Research Professor. During that time, Dr. Son focused on designing a peptide fragment of LIME capable of inducing activation induced cell death in an animal model of autoimmune disease. She had the opportunity to mentor ...
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In this project, we aimed to study on the immunological surveillance mechanisms against tumor cells using naturally occurring tumor models in mice. The major achievements were as follows. (0 We found that SPA-1 KO mice naturally develop a spectrum of myeloproliferative disorders including chronic myeloid leukemia of long latency. The diseases highly resembled human myeloproliferative diseases, and SPA-1 KO mice were considered to provide an excellent model to study the roles of immune system during the naturally occurring malignancy (2) It was found that SPA-1 KO mice gradually developed CD4 T cell dysfunction preceding the leukemia development, and it was suggested that the T cell dysfunction during the preleukemic stage might contribute to the frank leukemia development (3) After overt development of systemic leukemia, the mice rapidly developed severe CD4 T cell unresponsiveness. This was ascribed to the progressive increase in PD-1+ CD4 T cells with memory phenotype, which were totally ...
On screening of 138 haematological patients who had been in contact with an infectious TB case, a significantly higher rate of positive T-SPOT.TBTM test results compared with TST screening was found. The T-SPOT.TBTM test was positive in 44.2% of the contacts versus 17.4% for the TST. It was important to determine whether the higher apparent prevalence of infection found with the T-SPOT.TBTM test was due to the TST being falsely negative due to anergy, or to the T-SPOT.TBTM test being falsely positive in a number of patients.. The present data, although clearly not definitive, support the former view that the T-SPOT.TBTM test was correctly identifying infected patients anergic to the TST. First, the results demonstrate that the T-SPOT.TBTM test result was not affected by the WBC counts of the patients, whereas the TST results were affected by increasing immunosuppression. The response to the positive control mitogen in the T-SPOT.TBTM assay provided a control against anergy (notwithstanding the ...

Clonal anergy - WikipediaClonal anergy - Wikipedia

Jenkins, Marc K. (February 1992). "The role of cell division in the induction of clonal anergy". Immunology Today. 13 (2): 69- ... Clonal anergy at the US National Library of Medicine Medical Subject Headings (MeSH). ... Strong stimulation of T-cells either by IL-2 or by TCR/costimulatory receptors can break the anergy. Anergy may be taken ... Various chemicals inducing/inhibiting described T cell signalling pathways can be used to study the anergy. The anergy in T ...
more infohttps://en.wikipedia.org/wiki/Clonal_anergy

A cell culture model for T lymphocyte clonal anergy | ScienceA cell culture model for T lymphocyte clonal anergy | Science

... enters an unresponsive state known as clonal anergy in which the T cell is incapable of producing its own growth hormone, ...
more infohttp://science.sciencemag.org/content/248/4961/1349

A cell culture model for T lymphocyte clonal anergy | ScienceA cell culture model for T lymphocyte clonal anergy | Science

... enters an unresponsive state known as clonal anergy in which the T cell is incapable of producing its own growth hormone, ...
more infohttps://science.sciencemag.org/content/248/4961/1349?ijkey=07bc6242215839b8d499b0c732d5600b87d759d0&keytype2=tf_ipsecsha

Clonal anergy | definition of Clonal anergy by Medical dictionaryClonal anergy | definition of Clonal anergy by Medical dictionary

Clonal anergy explanation free. What is Clonal anergy? Meaning of Clonal anergy medical term. What does Clonal anergy mean? ... Looking for online definition of Clonal anergy in the Medical Dictionary? ... anergy. (redirected from Clonal anergy). Also found in: Dictionary, Thesaurus, Encyclopedia, Wikipedia. anergy. [an´er-je] 1. ... Clonal anergy , definition of Clonal anergy by Medical dictionary https://medical-dictionary.thefreedictionary.com/Clonal+ ...
more infohttp://medical-dictionary.thefreedictionary.com/Clonal+anergy

Nonmitogenic Anti-CD3 Monoclonal Antibodies Deliver a Partial T Cell Receptor Signal and Induce Clonal Anergy | JEMNonmitogenic Anti-CD3 Monoclonal Antibodies Deliver a Partial T Cell Receptor Signal and Induce Clonal Anergy | JEM

Nonmitogenic Anti-CD3 Monoclonal Antibodies Deliver a Partial T Cell Receptor Signal and Induce Clonal Anergy. Judith A. Smith ... Nonmitogenic Anti-CD3 Monoclonal Antibodies Deliver a Partial T Cell Receptor Signal and Induce Clonal Anergy ... 1993) Induction of T-cell anergy by altered T-cell-receptor ligand on live antigen-presenting cells. Nature (Lond) 363:156-159 ... 1994) Partial T cell signaling: altered phospho-zeta and lack of ZAP-70 recruitment in APL-induced T cell anergy. Cell 79:913- ...
more infohttp://jem.rupress.org/content/185/8/1413

Clonal anergy blocks in vivo growth of mature T cells and can be reversed in the absence of antigen. | JEMClonal anergy blocks in vivo growth of mature T cells and can be reversed in the absence of antigen. | JEM

Clonal anergy blocks in vivo growth of mature T cells and can be reversed in the absence of antigen.. B Rocha, C Tanchot, H Von ... Clonal anergy blocks in vivo growth of mature T cells and can be reversed in the absence of antigen. ... Here we show that in vivo the anergy can be reversed in the absence of antigen, such that the cells are then able to ... of reactive lymphocytes as well as from anergy. We have previously reported that mature CD4-CD8+ T cells when confronted with ...
more infohttp://jem.rupress.org/content/177/5/1517

Fas/fas ligand pathway, apoptosis, and clonal anergy involved in systemic acetylcholine receptor T cell epitope tolerance<...Fas/fas ligand pathway, apoptosis, and clonal anergy involved in systemic acetylcholine receptor T cell epitope tolerance<...

Deng C, Goluszko E, Christadoss P. Fas/fas ligand pathway, apoptosis, and clonal anergy involved in systemic acetylcholine ... The findings implicate the possible role of Fas-/Fas ligand-mediated apoptosis and the resulting clonal anergy as the ... Fas/fas ligand pathway, apoptosis, and clonal anergy involved in systemic acetylcholine receptor T cell epitope tolerance. / ... The findings implicate the possible role of Fas-/Fas ligand-mediated apoptosis and the resulting clonal anergy as the ...
more infohttps://researchexperts.utmb.edu/en/publications/fasfas-ligand-pathway-apoptosis-and-clonal-anergy-involved-in-sys

Induction of Tolerance: Overview, Central (Intrathymic) Mechanisms of Tolerance, Peripheral (Nonthymic) Mechanisms of ToleranceInduction of Tolerance: Overview, Central (Intrathymic) Mechanisms of Tolerance, Peripheral (Nonthymic) Mechanisms of Tolerance

Clonal anergy. T lymphocytes require 2 signals to become activated, to proliferate, and to differentiate. The first is the ... 12] The study showed that clonal deletion of host-reactive T cells was a major mechanism responsible for tolerance. [12] ... Lack of costimulation causes anergy; that is, T cells fail to respond to the MHC-peptide complex and remain unresponsive to ...
more infohttps://emedicine.medscape.com/article/430449-overview

Strong T cell tolerance in parent----F1 bone marrow chimeras prepared with supralethal irradiation. Evidence for clonal...Strong T cell tolerance in parent----F1 bone marrow chimeras prepared with supralethal irradiation. Evidence for clonal...

Evidence for clonal deletion and anergy. E K Gao E K Gao ... Evidence for clonal deletion and anergy.. J Exp Med 1 April ... it is suggested that T cell contact with thymic epithelial cells induced clonal deletion of most of the host-reactive T cells ... we suggest that the thymic epithelial cells induced a temporary form of anergy in the remaining host-reactive thymocytes. This ...
more infohttps://rupress.org/jem/article-standard/171/4/1101/49898/Strong-T-cell-tolerance-in-parent-F1-bone-marrow

Regulation of the Immune Response Flashcards by heerak Kang | BrainscapeRegulation of the Immune Response Flashcards by heerak Kang | Brainscape

clonal deletion, clonal anergy, functional deletion, generation of suppressor or regulatory T cells, blocking of presentation ...
more infohttps://www.brainscape.com/flashcards/regulation-of-the-immune-response-1475334/packs/2856913

others  Flashcards by Anthos Christofides | Brainscapeothers Flashcards by Anthos Christofides | Brainscape

1. clonal deletion (bone marrow) 2. clonal anergy (periphery) 9 Whether an antigen will iduce tolerance rather than immunologic ...
more infohttps://www.brainscape.com/flashcards/others-5178666/packs/7620266

Molecular Mechanisms of Immunological Self-Recognition - 1st EditionMolecular Mechanisms of Immunological Self-Recognition - 1st Edition

Clonal Abortion versus Clonal Anergy. Clonal Abortion and Clonal Anergy Come of Age in the Molecular Era. The Genesis of High- ... 4 T Cell Anergy. Introduction. Cellular Characteristics. Biochemical Events Resulting from TCR Occupancy. Reversal of Anergy. ... The Deletion-Anergy Decision. Consequences of Deletion versus Anergy. References. 3 Tolerant Autoreactive B Lymphocytes in the ... Deletion or Anergy?. Does the Follicular Mantle Zone Serve as a Reform School for Wayward B Cells?. References. Part III ...
more infohttps://www.elsevier.com/books/molecular-mechanisms-of-immunological-self-recognition/alt/978-0-12-053750-1

Autoimmunity - WikipediaAutoimmunity - Wikipedia

Clonal Anergy theory, proposed by Nossal, in which self-reactive T- or B-cells become inactivated in the normal individual and ... "Clonal anergy: the universally anergic B lymphocyte". Proceedings of the National Academy of Sciences of the United States of ... Clonal Deletion theory, proposed by Burnet, according to which self-reactive lymphoid cells are destroyed during the ... Clonal Ignorance theory, according to which autoreactive T cells that are not represented in the thymus will mature and migrate ...
more infohttps://en.wikipedia.org/wiki/Autoimmune

The Jun Kinase Cascade Is Responsible for Activating the CD28 Response Element of the IL-2 Promoter: Proof of Cross-Talk with...The Jun Kinase Cascade Is Responsible for Activating the CD28 Response Element of the IL-2 Promoter: Proof of Cross-Talk with...

Transactivation by AP-1 is a molecular target of T cell clonal anergy. Science 257: 1134. ... which has been ascribed to poorly identified anergy factors 7 . It has been proposed that these anergy factors are produced in ... CD28-mediated signaling co-stimulates murine T cells and prevents induction of anergy in T-cell clones. Nature 356: 607. ... Inhibition of mitogen-activated protein kinase kinase blocks T cell proliferation but does not induce or prevent anergy. J. ...
more infohttps://www.jimmunol.org/node/65696.full.print

The Use of Oral Tolerance in the Therapy of Chronic Inflamma... : Journal of Pediatric Gastroenterology and NutritionThe Use of Oral Tolerance in the Therapy of Chronic Inflamma... : Journal of Pediatric Gastroenterology and Nutrition

Evidence for clonal anergy. J Immunol 1991;147:2155-63. *Cited Here... , ... Induction of anergy or active suppression following oral tolerance is determined by antigen dosage. Proc Natl Acad Sci 1994;91: ... feeding regimenns induced the activation of regulatory cells whereas higher doses resulted in deletion or induction of anergy ...
more infohttp://journals.lww.com/jpgn/pages/articleviewer.aspx?year=2004&issue=06003&article=00015&type=fulltext

Crry/p65, a Membrane Complement Regulatory Protein, Has Costimulatory Properties on Mouse T Cells | The Journal of ImmunologyCrry/p65, a Membrane Complement Regulatory Protein, Has Costimulatory Properties on Mouse T Cells | The Journal of Immunology

T cell clonal anergy. Curr. Opin. Immunol. 9: 351. OpenUrlCrossRefPubMed ... The integration of these signals determines which activation pathways will be triggered, resulting in full activation, anergy, ...
more infohttps://www.jimmunol.org/content/164/9/4533?ijkey=aa8039857c7b911f60b5056d80bd08a4e5080abb&keytype2=tf_ipsecsha

Immunology for Life Scientists. 2nd EditionImmunology for Life Scientists. 2nd Edition

Clonal deletion.. Clonal anergy.. Clonal exhaustion.. Clonal abortion.. Antibody forming cell (AFC) blockade. ...
more infohttps://www.researchandmarkets.com/reports/2180853/immunology_for_life_scientists_2nd_edition

Molecular regulation of T-cell anergy. - Semantic ScholarMolecular regulation of T-cell anergy. - Semantic Scholar

One negative regulatory mechanism is clonal anergy, which is a hyporesponsive state that occurs when T cells are activated ... and the E3 ubiquitin ligases known as gene related to anergy in lymphocytes (GRAIL) and Casitas B-cell lymphoma-b (Cbl-b). A ... Adaptive tolerance and clonal anergy are distinct biochemical states.. *Lynda Chiodetti, Seeyoung Choi, Daniel L Barber, Ronald ... One negative regulatory mechanism is clonal anergy, which is a hyporesponsive state that occurs when T cells are activated ...
more infohttps://www.semanticscholar.org/paper/Molecular-regulation-of-T-cell-anergy.-Zheng-Zha/01409cb5019396d83a8f81a4c4c72c1897a5f172

Primary High-Dose Murine Norovirus 1 Infection Fails To Protect from Secondary Challenge with Homologous Virus | Journal of...Primary High-Dose Murine Norovirus 1 Infection Fails To Protect from Secondary Challenge with Homologous Virus | Journal of...

Evidence for clonal anergy. J. Immunol. 147:2155-2163.. OpenUrlAbstract. *↵ Wobus, C. E., S. M. Karst, L. B. Thackray, K.-O. ... Induction of anergy or active suppression following oral tolerance is determined by antigen dosage. Proc. Natl. Acad. Sci. USA ...
more infohttps://jvi.asm.org/content/83/13/6963.full?view=long&pmid=19403675

NFAT1 Supports Tumor-induced Anergy of CD4+ T Cells | Cancer ResearchNFAT1 Supports Tumor-induced Anergy of CD4+ T Cells | Cancer Research

B16-OVA-specific CD4+ T cells activate an anergy-associated program of gene expression characteristic of clonal anergy. To ... Clonal anergy in CD4+ T cells is established as a result of the activation of a program of gene expression that is dependent on ... Adaptive tolerance and clonal anergy are distinct biochemical states. J Immunol 2006;176:2279-91. ... In CD4+ T cells, clonal anergy occurs when the T-cell receptor is activated in the absence of a costimulatory signal. Here we ...
more infohttp://cancerres.aacrjournals.org/content/72/18/4642

Autoimmunity - WikipediaAutoimmunity - Wikipedia

Clonal Anergy theory, proposed by Nossal, in which self-reactive T- or B-cells become inactivated in the normal individual and ... "Clonal anergy: the universally anergic B lymphocyte". Proceedings of the National Academy of Sciences of the United States of ... Clonal Deletion theory, proposed by Burnet, according to which self-reactive lymphoid cells are destroyed during the ... Clonal Ignorance theory, according to which autoreactive T cells that are not represented in the thymus will mature and migrate ...
more infohttps://en.m.wikipedia.org/wiki/Autoimmune

Immunological Tolerance: MechanismsImmunological Tolerance: Mechanisms

Several mechanisms are involved in induction and maintenance of tolerance, including clonal deletion, clonal anergy, receptor ... Clonal anergy. In this tolerance mechanism, a self‐reactive B cell encountering its target autoantigen will undergo a state of ... Nossal GJ and Pike BL (1980) Clonal anergy: persistence in tolerant mice of antigen‐binding B lymphocytes incapable of ... Clonal deletion. The fate of B lymphocytes is governed by the specificity of their receptors. Encounter of a self‐reactive B ...
more infohttp://www.els.net/WileyCDA/ElsArticle/refId-a0000950.html

Dr. John E. Harris, Director of vitiligo clinical care and researchDr. John E. Harris, Director of vitiligo clinical care and research

Thesis Title: "The Molecular Mechanisms of T cell Clonal Anergy". Advisors: Dr. Aldo Rossini, Dr. Michael Czech. M.D., UMass ... Early growth response gene-2, a zinc-finger transcription factor, is required for full induction of clonal anergy in CD4+ T ... Depletion of the Programmed Death-1 Receptor completely reverses established clonal anergy in CD4+ T lymphocytes via an ...
more infohttps://www.umassmed.edu/vitiligo/about/director-john-e-harris-md-phd/
  • The findings implicate the possible role of Fas-/Fas ligand-mediated apoptosis and the resulting clonal anergy as the mechanisms of high dose AChR α146-162 peptide-induced tolerance on CD4 cells. (utmb.edu)
  • This process - called "clonal expansion" - allows the body to quickly mobilise an army of clones, as and when required. (wikipedia.org)
  • Not only did biochemical signals delivered by nonmitogenic anti-CD3 resemble altered peptide ligand signaling, but exposure of Th1 clones to nonmitogenic anti-CD3 also resulted in functional anergy. (rupress.org)
  • In the absence of the latter signal, the T cell makes only a partial response and, more importantly, enters an unresponsive state known as clonal anergy in which the T cell is incapable of producing its own growth hormone, interleukin-2, on restimulation. (sciencemag.org)
  • T-cell anergy can arise when the T-cell does not receive appropriate co-stimulation in the presence of specific antigen recognition. (wikipedia.org)
  • B-cell anergy can be induced by exposure to soluble circulating antigen, and is often marked by a downregulation of surface IgM expression and partial blockade of intracellular signaling pathways. (wikipedia.org)
  • Molecular regulation of T-cell anergy. (semanticscholar.org)
  • By illustrating the dependence of tumor-induced CD4+ T-cell anergy on NFAT1, our findings open the possibility of targeting this transcription factor to improve the efficacy of cancer immunotherapy or immunochemotherapy. (aacrjournals.org)
  • Controls the development of T cell clonal anergy by ubiquitination. (abcam.com)