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.
A HLA-DR antigen that is associated with HLA-DRB1 CHAINS encoded by DRB1*07 alleles.
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.
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 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)
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.
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.
A soluble substance elaborated by antigen- or mitogen-stimulated T-LYMPHOCYTES which induces DNA synthesis in naive lymphocytes.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
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.
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)
White blood cells formed in the body's lymphoid tissue. The nucleus is round or ovoid with coarse, irregularly clumped chromatin while the cytoplasm is typically pale blue with azurophilic (if any) granules. Most lymphocytes can be classified as either T or B (with subpopulations of each), or NATURAL KILLER CELLS.
Degeneration of distal aspects of a nerve axon following injury to the cell body or proximal portion of the axon. The process is characterized by fragmentation of the axon and its MYELIN SHEATH.
Lists of words, usually in alphabetical order, giving information about form, pronunciation, etymology, grammar, and meaning.
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 protein tyrosine kinase that is required for T-CELL development and T-CELL ANTIGEN RECEPTOR function.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
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.
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).
A family of the suborder HAPLORHINI comprising only one genus, HYLOBATES (also called Nomascus or Symphalangus).
The branch of psychology concerned with similarities or differences in the behavior of different animal species or of different races or peoples.
A sucrose polymer of high molecular weight.
Lack of correspondence between the way a stimulus is commonly perceived and the way an individual perceives it under given conditions.
A person's view of himself.
The knowledge or perception that someone or something present has been previously encountered.
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.
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)
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.
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)
Glycoproteins found on the membrane or surface of cells.
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.
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).
A medical specialty concerned with maintaining health and providing medical care to children from birth to adolescence.
An encapsulated lymphatic organ through which venous blood filters.
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.
An albumin obtained from the white of eggs. It is a member of the serpin superfamily.
Disorders that are characterized by the production of antibodies that react with host tissues or immune effector cells that are autoreactive to endogenous peptides.
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.
The teaching staff and members of the administrative staff having academic rank in a medical school.
A medical specialty concerned with the skin, its structure, functions, diseases, and treatment.
Educational institutions for individuals specializing in the field of medicine.
A strain of Rattus norvegicus which is a model for spontaneous insulin-dependent diabetes mellitus (DIABETES MELLITUS, INSULIN-DEPENDENT).
Time period from 1901 through 2000 of the common era.
The mechanism, in central lymphoid organs (THYMUS; BONE MARROW), that prevents immature lymphocytes from reacting to SELF-ANTIGENS. This is accomplished by CLONAL ANERGY and CLONAL DELETION.
An organism that, as a result of transplantation of donor tissue or cells, consists of two or more cell lines descended from at least two zygotes. This state may result in the induction of donor-specific TRANSPLANTATION TOLERANCE.
The occurrence in an individual of two or more cell populations of different chromosomal constitutions, derived from different individuals. This contrasts with MOSAICISM in which the different cell populations are derived from a single individual.
Transplantation between individuals of the same species. Usually refers to genetically disparate individuals in contradistinction to isogeneic transplantation for genetically identical individuals.
An induced state of non-reactivity to grafted tissue from a donor organism that would ordinarily trigger a cell-mediated or humoral immune response.
The transference of BONE MARROW from one human or animal to another for a variety of purposes including HEMATOPOIETIC STEM CELL TRANSPLANTATION or MESENCHYMAL STEM CELL TRANSPLANTATION.

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)

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 ...
TY - JOUR. T1 - Transcriptional modulation of TCR, Notch and Wnt signaling pathways in SEB-anergized CD4+ T cells. AU - Kurella, S.. AU - Yaciuk, J. C.. AU - Dozmorov, I.. AU - Frank, M. B.. AU - Centola, M.. AU - Farris, A. D.. PY - 2005/10/1. Y1 - 2005/10/1. N2 - Gene expression changes in CD4 + Vβ8+ T cells anergized by in vivo exposure to staphylococcal enterotoxin B (SEB) bacterial superantigen compared to CD4 + Vβ8+ nonanergic T cells were assessed using DNA microarrays containing 5184 murine complementary DNAs. Anergy in splenic T cells of SEB-immunized BALB/c mice was verified by dramatically reduced proliferative capacity and an 8 × overexpression of GRAIL mRNA in CD4 + Vβ8+ T cells taken from mice 7 days after injection. At an Associative t-test threshold of P,0.0005, 96 genes were overexpressed or detected only in anergic T cells, while 256 genes were suppressed or not detected in anergic T cells. Six of eight differential expressions tested using real-time quantitative PCR were ...
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 ...
Abstract. B cells are well-known mediators of humoral immunity and serve as costimulators in the generation of T cell-mediated responses. In several mouse model
Mice carrying the (TcrHEL3A9) transgene express the alpha and beta chains of a T-cell receptor specific for hen egg lysozyme. Transgenics are used to study maintenance and breakdown of immunological tolerance, overcoming of the anergic state, and issues of costimuli.
The E3 ligases GRAIL and Cbl-b are necessary for the induction of CD4+ T cell anergy. Using CD4+ T cells from wildtype (WT) and Cbl-b knockout (Cbl-B -/-) mice, we investigated the relationship between GRAIL and Cbl-b ...
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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 ...
Oral tolerance is a long recognized method to induce peripheral immune tolerance. The primary mechanisms by which orally administered antigen induces tolerance are via the generation of active suppression or clonal anergy. Low doses of orally administered antigen favor active suppression whereas hig …
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
El seminario titulado Mecanismos moleculares que regulan la tolerancia en los linfocitos T. Relevancia para el desarrollo de inmunoterapia será impartido por el Dr. Fernando Macian el próximo lunes 7 de septiembre de 2015 a partir de las 13.00 h. en el Salón de Actos del edificio del Instituto de Investigación Sanitaria INCLIVA. Macian Lab (overview): The antigen receptors of T cells recognize not only antigens derived from pathogenic cells and organisms, but also self-antigens expressed on the bodys own tissues. In healthy individuals, self-antigens do not elicit a significant immune response. Self-reactive lymphocytes are clonally eliminated during development and cells that survive this process are rendered tolerant in the periphery. Two of the major of the mechanisms responsible for peripheral T cell tolerance are anergy, an intracellular process in which antigen receptors become uncoupled from their downstream signaling pathways, and regulatory T cells, a population of T cells with the
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 ...
Grail raises $300 million in Series C round to give massive boost to the development of its liquid biopsy applications for cancer.
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 ...
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 provision of
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 ...
TY - JOUR. T1 - Anergy for delayed-type hypersensitivity in preleukemic akr mic1, 2. AU - Burdick, James F.. AU - Williams, G. Melville. N1 - Funding Information: I Received July 3, 1984; accepted November 27, 1984. 2Supported by Public Health Service grant AI-1508l from the National Institute of Allergy and Infectious Diseases, National Institutes of Health, and by Johns Hopkins University Institutional Research Grant RR·05378·l7. 3 Department of Surgery, Division of Transplantation and Vascular Surgery, The Johns Hopkins Hospital, 600 North Wolfe St., Baltimore, MD 21205. 4 4-(2-Hydroxyethyl)-I-piperazine ethanesulfonic acid. Copyright: Copyright 2016 Elsevier B.V., All rights reserved.. PY - 1985/5/1. Y1 - 1985/5/1. N2 - A singular anergy for delayed-type hypersensitivity (DTH) in preleukemic AKR mice was discovered. This total anergy for DTH against allogeneic cells, which developed in the AKR mice by 4 to 5 months of age, was not due to an artifact of route of sensitization or of other ...
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, ...
IntelliJ IDEA enables easy creation of the Grails or Griffon Application elements in the modules of the corresponding type (domain classes, controllers, scripts etc.) You can create new elements using the application-specific Grails or Griffon tool windows, or the Project tool window. Execution of the target that corresponds to the selected element type, is displayed in the console.. ...
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Sarcoidosis is a systemic granulomatous disease predominantly affecting the lungs. It is believed to be caused by exposure to pathogenic antigens in genetically susceptible individuals but the causative antigen has not been identified. The formation of non-caseating granulomas at sites of ongoing inflammation is the key feature of the disease. Other aspects of the pathogenesis are peripheral T-cell anergy and disease progression to fibrosis. Many T-cell-associated cytokines have been implicated in the immunopathogenesis of sarcoidosis, but it is becoming apparent that IL-12 cytokine family members including IL-12, IL-23, IL-27, and IL-35 are also involved. Although the members of this unique cytokine family are heterodimers of similar subunits, their biological functions are very diverse. Whilst IL-23 and IL-12 are pro-inflammatory regulators of Th1 and Th17 responses, IL-27 is bidirectional for inflammation and the most recent family member IL-35 is inhibitory. This review will discuss the current
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
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
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Laboratory of Dr. Dan Mueller. Research Emphasis/Pubications: Tolerance and autoimmunity - Rheumatoid arthritis, Epigenetics: Molecular mechanisms of transcriptional regulation in anergic and effector CD4+ T-cells. Differential gene expression profiles associated with the induction of clonal anergy. Gene expression profile analysis of CD4+ T follicular helper (Tfh) cells vs CD4+ T helper (Th) cells. List of all Publications. Current Position: Assistant Professor, Pediatrics-Allergy & Immunology, Baylor College of Medicine and Director, Primary Immunodeficiency Diseases Clinical Immunology Laboratory, Pediatrics Allergy, Immunology and Rheumatology, Texas Childrens Hospital, Houston, ...
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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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 ...
... 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 99 percent of ...
Both clonal anergy and clonal deletion have been shown to operate in vetoed T cells. The veto cell need only carry the self-MHC ... Avoiding self-reactivity in the T cell compartment is maintained by: clonal deletion in the thymus and suppressive cells that ...
Also was shown its role in T-cell clonal anergy downstream of Egr2, where NDRG1 is upregulated in the absence of costimulation ... October 2015). "Ndrg1 is a T-cell clonal anergy factor negatively regulated by CD28 costimulation and interleukin-2". Nature ...
This can induce T cell clonal deletion, T cell anergy or the proliferation of regulatory T cells (Tregs). Collectively, these ...
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 ...
This phenomenon results in T cells anergy. Repetitive stimulation of T cells by iDCs can convert them into Tregs Immature and ... Tolerogenic DCs are essential in maintenance of central and peripheral tolerance through induction of T cell clonal deletion, T ... These tolerogenic effects are mostly mediated through regulation of T cells such as inducing T cell anergy, T cell apoptosis ... cell anergy and generation and activation of regulatory T (Treg) cells. For that reason, tolerogenic DCs are possible ...
... 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 ...
... clonal anergy MeSH G04.610.484.120 - clonal deletion MeSH G04.610.484.800 - self tolerance MeSH G04.610.484.910 - tachyphylaxis ...
Clonal anergy Clonal deletion Clonal selection Clone (cell biology) CMKLR1 Colony stimulating factor 1 receptor Colony- ...
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 ...
... clonal deletion, receptor editing, anergy, or ignorance (B cell ignores signal and continues development). This negative ...
... 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 ... Clone (genetics) This disambiguation page lists articles associated with the title Clonal. If an internal link led you here, ...
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 ...
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 ...
Antigen-specific mechanisms of peripheral tolerance include direct inactivation of effector T cells by either clonal deletion, ... and so anergy will result if there is an MHC-TCR interaction between the T cell and the APC. Since many pathways of immunity ... conversion to regulatory T cells (Tregs) or induction of anergy. Tregs, which are also generated during thymic T cell ...
Clonal anergy) · படியாக்க நீக்கம் (Clonal deletion) · கர்ப்பத்‌தில் நோயெதிர்ப்புப் பொறுதி (Immune tolerance in pregnancy) · ...
Clonal anergy) · படியாக்க நீக்கம் (Clonal deletion) · கர்ப்பத்‌தில் நோயெதிர்ப்புப் பொறுதி (Immune tolerance in pregnancy) · ...
Clonal anergy. *Clonal deletion. *Tolerance in pregnancy. *Immunodeficiency. Immunogenetics. *Affinity maturation *Somatic ...
Clonal anergy. *Clonal deletion. *Tolerance in pregnancy. *Immunodeficiency. *Immune privilege. Immunogenetics. *Affinity ...
... because it is rapidly activated and does not require T cell help or clonal maturation and expansion. An example of TI-1 antigen ...
Clonal anergy. *Clonal deletion. *Tolerance in pregnancy. *Immunodeficiency. *Immune privilege. Immunogenetics. *Affinity ...
Clonal anergy. *Clonal deletion. *Tolerance in pregnancy. *Immunodeficiency. Immunogenetics. *Affinity maturation *Somatic ...
Clonal anergy. *Clonal deletion. *Tolerance in pregnancy. *Immunodeficiency. Immunogenetics. *Affinity maturation *Somatic ...
Circulating antibodies are produced by clonal B cells that specifically respond to only one antigen (an example is a virus ... This recombinational process that produces clonal antibody paratope diversity is called V(D)J or VJ recombination. Basically, ... where the genes are randomly recombined together is the hyper variable region used to recognise different antigens on a clonal ...
Tonn T, Becker S, Esser R, Schwabe D, Seifried E (August 2001). "Cellular immunotherapy of malignancies using the clonal ...
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 ...
Clonal anergy. *Clonal deletion. *Tolerance in pregnancy. *Immunodeficiency. Immunogenetics. *Affinity maturation *Somatic ...
The result is that even a clonal population of pathogens expresses a heterogeneous phenotype.[5] Many of the proteins known to ...
Clonal anergy. *Clonal deletion. *Tolerance in pregnancy. *Immunodeficiency. Immunogenetics. *Affinity maturation *Somatic ...
Myriad receptors are produced through a process known as clonal selection.[1][2] According to the clonal selection theory, at ... which builds on the existing clonal selection hypothesis and since 1974 has been developed mainly by Niels Jerne and Geoffrey W ... the CTL undergoes a process called clonal selection, in which it gains functions and divides rapidly to produce an army of " ...
B7/CD28 in central tolerance: costimulation promotes maturation of regulatory T cell precursors and prevents their clonal ... Increased circulating regulatory T cells (CD4(+)CD25 (+)CD127 (-)) contribute to lymphocyte anergy in septic shock patients. „ ...
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 ...
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 ...
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.[10] Burnet and Medawar were ultimately credited for "the discovery of acquired immune tolerance" ... Upregulation of cAMP after contact, inducing anergy (reduced proliferation and IL-2 signaling) ... or by induction of anergy, a state of non-activity.[16] Weakly autoreactive B cells may also remain in a state of immunological ...
Clonal anergy. *Clonal deletion. *Tolerance in pregnancy. *Immunodeficiency. Immunogenetics. *Affinity maturation *Somatic ...
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 ...
Clonal selection[edit]. For more details on lymph nodes, germinal centers of lymph nodes and clonal selection of B cells, see ... The clonal selection theory was proved correct when Sir Gustav Nossal showed that each B cell always produces only one antibody ... Schematic diagram to explain mechanisms of clonal selection of B cell[8] ... gave rise to the clonal selection theory, which proved all the elements of Ehrlich's hypothesis except that the specific ...
April 2007). "Limited peripheral T cell anergy predisposes to retinal autoimmunity". Journal of Immunology. 178 (7): 4276-83. ... 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 ...
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 ...
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 ...
... enters an unresponsive state known as clonal anergy in which the T cell is incapable of producing its own growth hormone, ...
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+ ...
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- ...
Clonal anergy is induced in vitro by T cell receptor occupancy in the absence of proliferation.. D R DeSilva, K B Urdahl and M ... Clonal anergy is induced in vitro by T cell receptor occupancy in the absence of proliferation. ... Clonal anergy is induced in vitro by T cell receptor occupancy in the absence of proliferation. ... Clonal anergy is induced in vitro by T cell receptor occupancy in the absence of proliferation. ...
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 ...
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 ...
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 ...
UV irradiation can induce in vitro clonal anergy in alloreactive cytotoxic T lymphocytes T Kobata, T Kobata ... T Kobata, H Ikeda, Y Ohnishi, N Urushibara, TA Takahashi, S Sekiguchi; UV irradiation can induce in vitro clonal anergy in ... 2/IL-2R signaling pathway are relevant to the clonal anergy induced in the alloreactive CTL by stimulation of UV-B-irradiated ...
5. Clonal Anergy and Tuning. *6. Extrinsic Controls of Self-Reactive Lymphocytes ...
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 ...
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 ...
Selective inactivation of cytotoxic T lymphocytes in long-term renal transplant recipients: Clonal anergy as a possible ... Selective inactivation of cytotoxic T lymphocytes in long-term renal transplant recipients: Clonal anergy as a possible ... Selective inactivation of cytotoxic T lymphocytes in long-term renal transplant recipients : Clonal anergy as a possible ... title = "Selective inactivation of cytotoxic T lymphocytes in long-term renal transplant recipients: Clonal anergy as a ...
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 ...
Clonal Anergy * Gene Expression * HLA Antigens / metabolism * Humans * Melanoma / genetics * Melanoma / immunology* ...
Clonal Anergy * Dendritic Cells / immunology* * Epitopes, T-Lymphocyte / immunology * Histocompatibility Antigens Class I / ... In particular, at the CD4+ cell level, IL-12 apparently acts as an adjuvant and an inhibitor of anergy induction. These data ...
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. ...
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 ...
clonal deletion, clonal anergy, functional deletion, generation of suppressor or regulatory T cells, blocking of presentation ...
1. clonal deletion (bone marrow) 2. clonal anergy (periphery) 9 Whether an antigen will iduce tolerance rather than immunologic ...
At every stage of the T cells journey, cell death exists as a checkpoint to limit clonal expansion and to terminate ... In the presence of co-stimulation-deficient T cell activation, anergy is a dominant hallmark that mandates T cell ... A number of T cell-intrinsic peripheral tolerance mechanisms (quiescence, ignorance, anergy, exhaustion, senescence and cell ... anergy, exhaustion, senescence and death. At the naive T cell stage, two intrinsic checkpoints that actively maintain tolerance ...
Clonal deletion.. Clonal anergy.. Clonal exhaustion.. Clonal abortion.. Antibody forming cell (AFC) blockade. ...
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 ...
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 ...
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 ...
CD2 is involved in maintenance and reversal of human alloantigen-specific clonal anergy. ... Complete blockade of B7 family-mediated costimulation is necessary to induce human alloantigen-specific anergy: a method to ...
Invest., 104:1715-1722, 1999), induction of clonal anergy (Dallman et al., J. Exp. Med., 173:79-87, 1991), cytokine production ...
T cell clonal anergy. Curr. Opin. Immunol. 9, 351-357 (1997).. OpenUrlCrossRefPubMedWeb of Science ... Homeostatic proliferation as an isolated variable reverses CD8+ T cell anergy and promotes tumor rejection. J. Immunol. 177, ... One potential immune inhibitory mechanism that might be more directly attributable to the tumor itself is T cell anergy (36). ... Interleukin-10-treated human dendritic cells induce a melanoma-antigen-specific anergy in CD8+ T cells resulting in a failure ...
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 ...
  • Anergy is one of three processes that induce tolerance, modifying the immune system to prevent self-destruction (the others being clonal deletion and immunoregulation). (wikipedia.org)
  • See Clonal anergy, Deletion. (thefreedictionary.com)
  • Experiments in various models have indicated that immunological tolerance can result from the physical elimination (deletion) of reactive lymphocytes as well as from anergy. (rupress.org)
  • Evidence for clonal deletion and anergy. (rupress.org)
  • To account for the residual host reactivity of LN CD4+ cells and the incomplete deletion of V beta 11+ cells, it is suggested that T cell contact with thymic epithelial cells induced clonal deletion of most of the host-reactive T cells but spared a proportion of these cells (possibly low affinity cells). (rupress.org)
  • Deletion or Anergy? (elsevier.com)
  • Clonal Deletion theory , proposed by Burnet , according to which self-reactive lymphoid cells are destroyed during the development of the immune system in an individual. (wikipedia.org)
  • 7 ) introduced the concept of low and high dose oral tolerance (analogous to systemic tolerance) where low dose feeding regimenns induced the activation of regulatory cells whereas higher doses resulted in deletion or induction of anergy in antigen reactive cells ( 8 ). (lww.com)
  • Bouneaud, C., Kourilsky, P. & Bousso, P. Impact of negative selection on the T cell repertoire reactive to a self-peptide: a large fraction of T cell clones escapes clonal deletion. (nature.com)
  • Theories of tolerance induction include clonal deletion and clonal anergy. (thefreedictionary.com)
  • In clonal deletion, the actual clone of cells is eliminated whereas in clonal anergy the cells are present but nonfunctional. (thefreedictionary.com)
  • The immune system evolved various mechanisms to constrain such autoreactive T cells and maintain peripheral tolerance, including T cell anergy, deletion, and suppression by regulatory T cells (T Regs ). (frontiersin.org)
  • Low doses of oral antigen induce active suppression, whereas high doses induce clonal anergy and deletion. (nih.gov)
  • Several mechanisms are involved in induction and maintenance of tolerance, including clonal deletion, clonal anergy, receptor editing, receptor down‐modulation and lymphocyte sequestration. (els.net)
  • T lymphocytes specific for self‐peptides bound to major histocompatibility complex peptides are eliminated by clonal deletion, a process known as negative selection. (els.net)
  • These approaches utilize various mechanisms of peripheral tolerance such as deletion, activation-induced cell death (AICD, apoptosis), anergy, immune deviation, and/or induction of regulatory T cells (Tregs). (frontiersin.org)
  • 12 , 16 Three fundamental mechanisms accounting for T-cell unresponsiveness have been described- peripheral clonal deletion, 17 clonal anergy, 18 and suppression/regulation 19 -which can also produce different T-cell phenotypes. (bloodjournal.org)
  • Self-directed lymphocytes may evade clonal deletion at ontogenesis but still remain harmless due to a mechanism called clonal anergy. (diva-portal.org)
  • The Thymus, site of clonal deletion, is very efficient in removing autoreactive T-cells. (bio.net)
  • Negative selection of autoreactive cells has been proposed to occur by clonal elimination or abortion (deletion), clonal silencing (anergy), and clonal alteration (receptor editing). (springer.com)
  • Rather than present a comprehensive review of the findings in this area, the authors will concentrate on the role of clonal deletion in the tolerization of immature B-cells. (springer.com)
  • Is clonal deletion necessary for the maintenance of B-cell tolerance? (springer.com)
  • Nemazee, D. A. and Burki, K. (1989) Clonal deletion of B lymphocytes in a transgenic mouse bearing anti-MHC class I antibody genes. (springer.com)
  • In the B‐lymphocyte compartment, tolerance to self‐components is maintained by four mechanisms: clonal ignorance, clonal anergy, clonal deletion and receptor editing. (els.net)
  • In addition to the elimination of self-reactive T cells in the thymus, tolerance is maintained in the periphery through clonal deletion, induction of anergy, and differentiation of regulatory T cells (Treg). (jimmunol.org)
  • The mechanism(s) of the TRIM effect(s) also remains elusive, and it is possible that a large number of biologic mechanisms may underlie the effect(s). 28-31 The infusion of foreign antigen in either a soluble 31-36 or cell-associated 37-43 form has been shown to induce immune suppression, anergy, and clonal deletion in studies in experimental animals. (bloodjournal.org)
  • tolerance or non-tolerance related to anergia, clonal deletion, and cellular suppression of CD8 lymphocytes, allergenic hypersensitivity reactions) ( Brandtzaeg. (signs-of-the-past.eu)
  • While it may increase sensitivity, treatment times longer than 8 weeks should be explained clearly and justified, since long treatment times may produce an apparent increase in mutant frequency through clonal expansion Anergy is one of three processes that induce tolerance, modifying the immune system to prevent self-destruction the others being clonal deletion and immunoregulation. (konradt.ru)
  • 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. (wikipedia.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)
  • Anergy can be induced in mature and differentiated CD4+ T cells by exposure to complexes of antigen and appropriate (self) MHC in absence of certain uncharacterised co-stimulatory signals on the antigen-presenting cells. (thefreedictionary.com)
  • In patients who have received blood transfusions, anergy may be induced by presentation of antigen by "nonprofessional" antigen-presenting cells. (thefreedictionary.com)
  • Clonal anergy blocks in vivo growth of mature T cells and can be reversed in the absence of antigen. (rupress.org)
  • Here we show that in vivo the anergy can be reversed in the absence of antigen, such that the cells are then able to proliferate extensively in vivo to a new challenge with the antigen in question. (rupress.org)
  • Specifically, in a murine model of melanoma, we found that cancer cells induced anergy in antigen-specific CD4+ T-cell populations, resulting in defective production of several key effector cytokines. (aacrjournals.org)
  • NFAT1 deficiency blunted the induction of anergy in tumor antigen-specific CD4+ T cells, enhancing antitumor responses. (aacrjournals.org)
  • Here, using a B16 melanoma tumor model expressing the tumor surrogate antigen chicken albumin (OVA), we show that tumor antigen specific CD4+ T cells are rendered anergic in vivo through a mechanism that requires NFAT1 activity and involves the expression of anergy specific genes. (aacrjournals.org)
  • This model explains the process of activation or anergy when a naive T cell confronts an antigen ( 1 , 2 ). (frontiersin.org)
  • One negative regulatory mechanism is clonal anergy, which is a hyporesponsive state that occurs when T cells are activated through the T-cell antigen receptor in the absence of appropriate co-stimulatory signals. (semanticscholar.org)
  • Therefore, SAgs stimulate both antigen-presenting cells (APCs) and T lymphocytes, which leads to the massive production of cytokines, enhanced expression and/or activation of cell adhesion molecules, T-cell proliferation, activation-induced apoptosis, and T-cell anergy. (arvojournals.org)
  • Whether levomilnacipran will show particular promise among subsets of depressed patients, such as those with prominent fatigue, anergiaThis page was last edited on 13 Mayat T-cell anergy can arise when the T-cell does not receive appropriate co-stimulation in the presence of specific antigen recognition. (signs-of-the-past.eu)
  • This phenomenon was first described in B lymphocytes by Gustav Nossal and termed "clonal anergy. (wikipedia.org)
  • A novel E3 ubiquitin ligase substrate screen identifies Rho guanine dissociation inhibitor as a substrate of gene related to anergy in lymphocytes. (semanticscholar.org)
  • For B-lymphocytes, two major explanations for anergy developed over the last decades: according to Varela theory, anergy stems from a proper orchestration of the whole B-repertoire, such that self-reactive clones, due to intensive feed-back from other clones, display strong inertia when mounting a response. (diva-portal.org)
  • Conversely, according to the model of cognate response, self-reacting cells are not stimulated by helper lymphocytes and the absence of such signaling yields anergy. (diva-portal.org)
  • After SEB injections, lymphocyte infiltration into the corneal grafts was reduced, and the expression of NK1.1 + lymphocytes was enhanced, suggesting that anergy may be occurring. (arvojournals.org)
  • The contributors discuss the elimination of autoreactive lymphocytes during their development in the thymus and bone marrow, the suppression of autoreactive cells by regulatory T cells in the periphery, and intrinsic mechanisms that produce clonal anergy. (cshlpress.com)
  • Dendritic cells (DC) in tumor microenvironments seem to play a crucial role in the induction of anergy in CD4+ T cells ( 9 ). (aacrjournals.org)
  • Although the tremendous clonal diversity expressed in the B-cell receptor (BCR) repertoire is beneficial for mounting immune responses to foreign antigens, it is simultaneously detrimental in that it may include a multitude of BCRs capable of recognizing self antigens. (springer.com)
  • Sallinen K, Veräjänkorva E, Pöllänen P. Expression of antigens involved in the presentation of lipid antigens and induction of clonal anergy in the female reproductive tract. (southernbiotech.com)
  • Anergy is a term in immunobiology that describes a lack of reaction by the body's defense mechanisms to foreign substances, and consists of a direct induction of peripheral lymphocyte tolerance. (wikipedia.org)
  • 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)
  • The data indicate first that clonal anergy at least in the Mls-1 SUP a system is controlled by hemopoietic cells, and second, that T cell unresponsiveness in vivo may in some cases depend on mechanisms other than clonal anergy, e. (konradt.ru)
  • These results suggest that downregulation of T-cell receptor (TCR) and impairment in the post-IL- 2/IL-2R signaling pathway are relevant to the clonal anergy induced in the alloreactive CTL by stimulation of UV-B-irradiated Sa cells. (ashpublications.org)
  • NFAT homodimers are directly responsible for the expression of anergy associated genes such as ubiquitin ligase GRAIL or a protease caspase 3. (wikipedia.org)
  • Here we report that the key T-cell transcription factor NFAT mediates expression of anergy-associated genes in the context of cancer. (aacrjournals.org)
  • Since these latter cells appeared to be functionally inert in the thymus (in contrast to LN), we suggest that the thymic epithelial cells induced a temporary form of anergy in the remaining host-reactive thymocytes. (rupress.org)
  • NKT cell anergy was induced in a thymus-independent manner and maintained in an NKT cell-autonomous manner. (jci.org)
  • The clonal expansion of those cells can lead to autoimmune diseases, wherein the body attacks itself. (wikipedia.org)
  • Once induced, anergy could be reversed if the T cells were allowed to undergo multiple rounds of cell division. (jimmunol.org)
  • In CD4+ T cells, clonal anergy occurs when the T-cell receptor is activated in the absence of a costimulatory signal. (aacrjournals.org)
  • Clonal anergy in CD4+ T cells is established as a result of the activation of a program of gene expression that is dependent on the transcription factor NFAT. (aacrjournals.org)
  • Furthermore, by specifically targeting the regulation of anergy induction using NFAT1-deficient mice, our results support that tumor-induced CD4+ T-cell anergy participates in the evasion of antitumor responses, as NFAT1-deficient T cells become resistant to tumor-induced anergy, delaying tumor appearance and slowing tumor growth. (aacrjournals.org)
  • Clonal anergy theory, proposed by Nossal, in which self-reactive T- or B-cells become inactivated in the normal individual and cannot amplify the immune response. (wikipedia.org)
  • Reversion of anergy signatures in clonal CD21low B cells of mixed cryoglobulinemia after clearance of HCV viremia. (nature.com)
  • Clonal expansion of immunoglobulin M+CD27+ B cells in HCV-associated mixed cryoglobulinemia. (nature.com)
  • Our group also discovered the B7-1 and B7-2 molecules that bind to the costimulatory CD28 and coinhibitory CTLA-4 receptor and provide the critical costimulatory signal for full T cell activation, clonal expansion, and development of effector function through their interaction with CD28 on T cells. (dana-farber.org)
  • Following T cell activation, the B7-1-B7-2 interaction with CTLA-4, expressed on activated T cells, leads to down-regulation of T cell activation, whereas stimulation of the TCR alone leads to T cell clonal anergy. (dana-farber.org)
  • Anergy is a functionally silent state induced in B cells and T cells, allowing them to persist functionally inactivated in tolerant animals. (els.net)
  • The proliferative unresponsiveness of the secondary SAg responder T cells has been termed anergy. (arvojournals.org)
  • Recently, E3 ubiquitin ligases have been shown to mediate the development of a durable state of unresponsiveness in T cells called clonal anergy. (biomedcentral.com)
  • Simpson, Michael Proffitt, E. New York and London: The clonal expansion of those cells can lead to autoimmune diseaseswherein the body attacks itself. (signs-of-the-past.eu)
  • Depletion, anergiadeflated ego-ideal structures Khantzian, The anergy in T cells can be induced by Ionomycinthe ionophore capable of raising intracellular concentration of calcium ions artificially. (signs-of-the-past.eu)
  • Clonal anergy is induced in vitro by T cell receptor occupancy in the absence of proliferation. (jimmunol.org)
  • 26 T cell receptor signals without co-stimulation result in a state of prolonged inactivation or anergy. (bmj.com)
  • Peripheral tolerance in T cell receptor-transgenic mice: evidence for T cell anergy. (semanticscholar.org)
  • In this Perspective, we discuss the mediators and networks that control the six main peripheral tolerance checkpoints throughout the life of a T cell: quiescence, ignorance, anergy, exhaustion, senescence and death. (nature.com)
  • This is called Clonal Ignorance. (bio.net)
  • Clonal ignorance is postulated to underlie NAb production. (els.net)
  • 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)
  • Anergy was induced when T cell clones were stimulated under conditions where both TCR occupancy and costimulatory signals were provided but where proliferation in response to the IL-2 produced was prevented. (jimmunol.org)
  • If MHC/AG is presented to the autoreactive T-cell but is not followed by costimulation, the result is Clonal anergy. (bio.net)
  • In the presence of co-stimulation-deficient T cell activation, anergy is a dominant hallmark that mandates T cell unresponsiveness. (nature.com)
  • Caracteristicas clinicas y factores de riesgo para tuberculosis en pacientes receptores de injerto renal. (signs-of-the-past.eu)
  • Aan de hand van data uit de literatuur en ons eigen laboratorium bekeken we een 300-tal moleculen die reeds in vivo of in vitro getest waren. (scriptiebank.be)
  • Isolated nucleic acid compositions and sequences of anergy associated genes are provided, including the novel GRAIL gene. (konradt.ru)
  • T-cell hyporesponsiveness can be caused by clonal anergy or adaptive tolerance, but the pathophysiological roles of these processes in specific tumor contexts has yet to be understood. (aacrjournals.org)
  • Adaptive tolerance and clonal anergy are distinct biochemical states. (semanticscholar.org)
  • Nossal, G. J. V. and Pike, B. L. (1975) Evidence for the clonal abortion theory of B-lymphocyte tolerance. (springer.com)
  • In this case NFAT homodimerizes (complexes with itself), working as a transcriptional factor that induces anergy in the lymphocyte instead. (wikipedia.org)
  • MSC-mediated inhibition induces an unresponsive T-cell profile that is fully consistent with that observed in division arrest anergy. (bloodjournal.org)
  • At the cellular level, "anergy" is the inability of an immune cell to mount a complete response against its target. (wikipedia.org)
  • Blocking of the pathway leading to the anergy can be also done by cyclosporin Awhich is capable of inhibiting calcineurin - the phosphatase responsible for dephosphorylating of NFAT priming its activation. (signs-of-the-past.eu)
  • Burnet, F.M. (1959) Clonal Selection Theory of Acquired Immunity Vanderbilt University, Nashville, TN. (springer.com)
  • The purpose of this study was to determine the optimal conditions for prolonging corneal allograft survival by inducing anergy with the superantigen staphylococcal enterotoxin B (SEB). (arvojournals.org)
  • In particular, at the CD4+ cell level, IL-12 apparently acts as an adjuvant and an inhibitor of anergy induction. (nih.gov)
  • 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)
  • Failure of the T cell to receive a second signal can lead to clonal anergy ( 2 ). (pnas.org)