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.
Inbred BALB/c mice are a strain of laboratory mice that have been selectively bred to be genetically identical to each other, making them useful for scientific research and experiments due to their consistent genetic background and predictable responses to various stimuli or treatments.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Clonal anergy is a term used in immunology to describe a state of immune tolerance or unresponsiveness in certain T cells, a type of white blood cell that plays a central role in the body's immune response. This condition arises when T cells are exposed to persistent antigens, such as those derived from viruses or tumors, and fail to become fully activated.

In normal circumstances, when a T cell encounters an antigen presented by an antigen-presenting cell (APC), it becomes activated and undergoes clonal expansion, producing many copies of itself that are specific for that particular antigen. These activated T cells then migrate to the site of infection or tissue damage and help coordinate the immune response to eliminate the threat.

However, in some cases, persistent exposure to an antigen can lead to a state of exhaustion or anergy in the T cells, where they are no longer able to respond effectively to that antigen. This is thought to occur due to chronic stimulation and activation of the T cells, which can lead to the upregulation of inhibitory receptors and the downregulation of activating receptors on their surface.

Clonal anergy is a mechanism by which the immune system attempts to prevent excessive or inappropriate immune responses that could cause tissue damage or autoimmunity. However, it can also be a barrier to effective immunotherapy for diseases such as cancer, where T cells need to be activated and able to recognize and eliminate tumor cells.

In summary, clonal anergy is a state of immune tolerance in certain T cells that have been persistently exposed to antigens, leading to their failure to become fully activated and respond effectively to those antigens.

HLA-DR7 antigen is a human leukocyte antigen (HLA) serotype that is part of the major histocompatibility complex (MHC) class II, which plays a crucial role in the immune system. The HLA-DR7 antigen is encoded by the DRB1*07 gene and is expressed on the surface of antigen-presenting cells such as B lymphocytes, monocytes, and dendritic cells.

The HLA-DR7 antigen presents peptide fragments to CD4+ T helper cells, which then activate other immune cells like B cells and cytotoxic T cells to mount an immune response against pathogens or infected cells. The HLA-DR7 serotype is relatively common in many populations, with varying frequencies depending on the ethnic background.

It's important to note that certain HLA types, including HLA-DR7, have been associated with increased susceptibility or resistance to various diseases, such as autoimmune disorders and infectious diseases. However, the relationship between HLA types and disease is complex and not fully understood, as it involves multiple genetic and environmental factors.

Immune tolerance, also known as immunological tolerance or specific immune tolerance, is a state of unresponsiveness or non-reactivity of the immune system towards a particular substance (antigen) that has the potential to elicit an immune response. This occurs when the immune system learns to distinguish "self" from "non-self" and does not attack the body's own cells, tissues, and organs.

In the context of transplantation, immune tolerance refers to the absence of a destructive immune response towards the transplanted organ or tissue, allowing for long-term graft survival without the need for immunosuppressive therapy. Immune tolerance can be achieved through various strategies, including hematopoietic stem cell transplantation, costimulation blockade, and regulatory T cell induction.

In summary, immune tolerance is a critical mechanism that prevents the immune system from attacking the body's own structures while maintaining the ability to respond appropriately to foreign pathogens and antigens.

T-lymphocytes, also known as T-cells, are a type of white blood cell that plays a key role in the adaptive immune system's response to infection. They are produced in the bone marrow and mature in the thymus gland. There are several different types of T-cells, including CD4+ helper T-cells, CD8+ cytotoxic T-cells, and regulatory T-cells (Tregs).

CD4+ helper T-cells assist in activating other immune cells, such as B-lymphocytes and macrophages. They also produce cytokines, which are signaling molecules that help coordinate the immune response. CD8+ cytotoxic T-cells directly kill infected cells by releasing toxic substances. Regulatory T-cells help maintain immune tolerance and prevent autoimmune diseases by suppressing the activity of other immune cells.

T-lymphocytes are important in the immune response to viral infections, cancer, and other diseases. Dysfunction or depletion of T-cells can lead to immunodeficiency and increased susceptibility to infections. On the other hand, an overactive T-cell response can contribute to autoimmune diseases and chronic inflammation.

A clone is a group of cells that are genetically identical to each other because they are derived from a common ancestor cell through processes such as mitosis or asexual reproduction. Therefore, the term "clone cells" refers to a population of cells that are genetic copies of a single parent cell.

In the context of laboratory research, cells can be cloned by isolating a single cell and allowing it to divide in culture, creating a population of genetically identical cells. This is useful for studying the behavior and characteristics of individual cell types, as well as for generating large quantities of cells for use in experiments.

It's important to note that while clone cells are genetically identical, they may still exhibit differences in their phenotype (physical traits) due to epigenetic factors or environmental influences.

1. Receptors: In the context of physiology and medicine, receptors are specialized proteins found on the surface of cells or inside cells that detect and respond to specific molecules, known as ligands. These interactions can trigger a range of responses within the cell, such as starting a signaling pathway or changing the cell's behavior. There are various types of receptors, including ion channels, G protein-coupled receptors, and enzyme-linked receptors.

2. Antigen: An antigen is any substance (usually a protein) that can be recognized by the immune system, specifically by antibodies or T-cells, as foreign and potentially harmful. Antigens can be derived from various sources, such as bacteria, viruses, fungi, parasites, or even non-living substances like pollen, chemicals, or toxins. An antigen typically contains epitopes, which are the specific regions that antibodies or T-cell receptors recognize and bind to.

3. T-Cell: Also known as T lymphocytes, T-cells are a type of white blood cell that plays a crucial role in cell-mediated immunity, a part of the adaptive immune system. They are produced in the bone marrow and mature in the thymus gland. There are several types of T-cells, including CD4+ helper T-cells, CD8+ cytotoxic T-cells, and regulatory T-cells (Tregs). T-cells recognize antigens presented to them by antigen-presenting cells (APCs) via their surface receptors called the T-cell receptor (TCR). Once activated, T-cells can proliferate and differentiate into various effector cells that help eliminate infected or damaged cells.

Lymphocyte activation is the process by which B-cells and T-cells (types of lymphocytes) become activated to perform effector functions in an immune response. This process involves the recognition of specific antigens presented on the surface of antigen-presenting cells, such as dendritic cells or macrophages.

The activation of B-cells leads to their differentiation into plasma cells that produce antibodies, while the activation of T-cells results in the production of cytotoxic T-cells (CD8+ T-cells) that can directly kill infected cells or helper T-cells (CD4+ T-cells) that assist other immune cells.

Lymphocyte activation involves a series of intracellular signaling events, including the binding of co-stimulatory molecules and the release of cytokines, which ultimately result in the expression of genes involved in cell proliferation, differentiation, and effector functions. The activation process is tightly regulated to prevent excessive or inappropriate immune responses that can lead to autoimmunity or chronic inflammation.

Interleukin-2 (IL-2) is a type of cytokine, which are signaling molecules that mediate and regulate immunity, inflammation, and hematopoiesis. Specifically, IL-2 is a growth factor for T cells, a type of white blood cell that plays a central role in the immune response. It is primarily produced by CD4+ T cells (also known as T helper cells) and stimulates the proliferation and differentiation of activated T cells, including effector T cells and regulatory T cells. IL-2 also has roles in the activation and function of other immune cells, such as B cells, natural killer cells, and dendritic cells. Dysregulation of IL-2 production or signaling can contribute to various pathological conditions, including autoimmune diseases, chronic infections, and cancer.

Transgenic mice are genetically modified rodents that have incorporated foreign DNA (exogenous DNA) into their own genome. This is typically done through the use of recombinant DNA technology, where a specific gene or genetic sequence of interest is isolated and then introduced into the mouse embryo. The resulting transgenic mice can then express the protein encoded by the foreign gene, allowing researchers to study its function in a living organism.

The process of creating transgenic mice usually involves microinjecting the exogenous DNA into the pronucleus of a fertilized egg, which is then implanted into a surrogate mother. The offspring that result from this procedure are screened for the presence of the foreign DNA, and those that carry the desired genetic modification are used to establish a transgenic mouse line.

Transgenic mice have been widely used in biomedical research to model human diseases, study gene function, and test new therapies. They provide a valuable tool for understanding complex biological processes and developing new treatments for a variety of medical conditions.

CD4-positive T-lymphocytes, also known as CD4+ T cells or helper T cells, are a type of white blood cell that plays a crucial role in the immune response. They express the CD4 receptor on their surface and help coordinate the immune system's response to infectious agents such as viruses and bacteria.

CD4+ T cells recognize and bind to specific antigens presented by antigen-presenting cells, such as dendritic cells or macrophages. Once activated, they can differentiate into various subsets of effector cells, including Th1, Th2, Th17, and Treg cells, each with distinct functions in the immune response.

CD4+ T cells are particularly important in the immune response to HIV (human immunodeficiency virus), which targets and destroys these cells, leading to a weakened immune system and increased susceptibility to opportunistic infections. The number of CD4+ T cells is often used as a marker of disease progression in HIV infection, with lower counts indicating more advanced disease.

BALB/c is an inbred strain of laboratory mouse that is widely used in biomedical research. The strain was developed at the Institute of Cancer Research in London by Henry Baldwin and his colleagues in the 1920s, and it has since become one of the most commonly used inbred strains in the world.

BALB/c mice are characterized by their black coat color, which is determined by a recessive allele at the tyrosinase locus. They are also known for their docile and friendly temperament, making them easy to handle and work with in the laboratory.

One of the key features of BALB/c mice that makes them useful for research is their susceptibility to certain types of tumors and immune responses. For example, they are highly susceptible to developing mammary tumors, which can be induced by chemical carcinogens or viral infection. They also have a strong Th2-biased immune response, which makes them useful models for studying allergic diseases and asthma.

BALB/c mice are also commonly used in studies of genetics, neuroscience, behavior, and infectious diseases. Because they are an inbred strain, they have a uniform genetic background, which makes it easier to control for genetic factors in experiments. Additionally, because they have been bred in the laboratory for many generations, they are highly standardized and reproducible, making them ideal subjects for scientific research.

Clonal+anergy at the U.S. National Library of Medicine Medical Subject Headings (MeSH) (Articles with short description, Short ... Jenkins MK (February 1992). "The role of cell division in the induction of clonal anergy". Immunology Today. 13 (2): 69-73. doi ... 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 ...
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 ... Clonal deletion theory, proposed by Burnet, according to which self-reactive lymphoid cells are destroyed during the ...
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 ... In immunology, clonal deletion is the removal through apoptosis of B cells and T cells that have expressed receptors for self ...
... 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 ...
... a model for how the immune system responds to infection Clonal anergy, a lack of reaction by the body's defense mechanisms to ... Look up clonal in Wiktionary, the free dictionary. Clonal may refer to: Clonal interference, a phenomenon that occurs when two ... also called clonal anemone Vegetative cloning, a form of asexual reproduction in plants Clonal reproduction Clonal deletion, a ... Cloning This disambiguation page lists articles associated with the title Clonal. If an internal link led you here, you may ...
... 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 ...
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 deletion, receptor editing, anergy, or ignorance (B cell ignores signal and continues development). This negative ...
Anergy is a state of functional unresponsiveness induced upon self antigen recognition. T-cells can be made non-responsive to ... ignorance of antigen and direct inactivation of effector T cells by either clonal deletion, conversion to regulatory T cells ( ... Anergy is reversible and T cells can recover their functional responsiveness in the absence of the antigen. After T cell ... Kalekar, Lokesh A.; Mueller, Daniel L. (2017-04-01). "Relationship between CD4 Tregs and anergy in vivo". Journal of Immunology ...
These costimulatory signals are necessary to prevent anergy and are provided by the interaction between CD80/CD86 and CD28 ... production of interleukin 2 and clonal expansion. Interaction between CD86 and CD28 activates mitogen-activated protein kinase ... suppress the immune response and lead to increased anergy. Since CTLA-4 binds to CD86 with higher affinity than CD28, the co- ...
Induction of anergy (a state of non-reactivity) T cell central tolerance occurs in the thymus. T cells undergo positive and ... If they bind a self peptide, then they are signaled to apoptose (process of clonal deletion). The thymic epithelial cells ... The results were explained by Burnet's clonal selection hypothesis. Burnet and Medawar won the Nobel Prize in 1960 for their ... clonal deletion) Receptor editing: the self-reactive B cell changes specificity by rearranging genes and develops a new BCR ...
In this case, in the absence of co-stimulatory signals, the interaction of dendritic and T cells leads to T cell anergy. The ... statements only suggest that loss of CD28 expression marks functional differentiation to cytotoxic memory cells within clonal ...
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 ...
Nature 333, 742-746 (1988); Swat, W., Ignatowicz, L., von Boehmer, H. and Kisielow, P.: Clonal deletion of immature CD4+8+ ... Science 251, 1225 (1991). Peripheral tolerance by deletion of and reversible anergy in matureT cells. Borgulya, P., Kishi, H., ...
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 ... allowing the cell to activate instead of undergoing anergy. The second signal is then obsolete; only the first signal is ...
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 ...
Kearney ER, Walunas TL, Karr RW, Morton PA, Loh DY, Bluestone JA, Jenkins MK (August 1995). "Antigen-dependent clonal expansion ... "CD28-mediated signalling co-stimulates murine T cells and prevents induction of anergy in T-cell clones". Nature. 356 (6370): ...
Clonal populations of CD8+ cytotoxic T cells have been grown which carry T cell receptors specific to influenza. These work ... The authors concluded that resistance to flu symptoms was associated with a shift in cell mediated immunity from anergy toward ...
Along with anergy and T-cell exhaustion, immunosenescence belongs among the major immune system dysfunctional states. However, ... shift in the CD4+/CD8+ ratio the accumulation and clonal expansion of memory and effector T cells impaired development of CD4+ ... Crespo J, Sun H, Welling TH, Tian Z, Zou W (April 2013). "T cell anergy, exhaustion, senescence, and stemness in the tumor ... while T-cell anergy is a reversible condition, as of 2020 no techniques for immunosenescence reversal had been developed. ...
Virtual memory T cells (TVM) differ from the other memory subsets in that they do not originate following a strong clonal ... T cell receptor signalling alone results in anergy. The signalling pathways downstream from co-stimulatory molecules usually ...
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 ...
Tonn T, Becker S, Esser R, Schwabe D, Seifried E (August 2001). "Cellular immunotherapy of malignancies using the clonal ... July 2016). "A novel TLR7 agonist reverses NK cell anergy and cures RMA-S lymphoma-bearing mice". Oncoimmunology. 5 (7): ... dependent manner thus reversing the NK cell anergy which ultimately lead to lysis of the tumor. VTX-2337 is a selective TLR-8 ...
Scientists Ernest A. McCulloch and James E. Till first revealed the clonal nature of marrow cells in the 1960s. In 1970, Dr. ... "Bone marrow mesenchymal stem cells induce division arrest anergy of activated T cells". Blood. 105 (7): 2821-7. doi:10.1182/ ... ISBN 978-1-4614-7696-2. Becker AJ, McCulloch EA, Till JE (February 1963). "Cytological demonstration of the clonal nature of ...
Myriad receptors are produced through a process known as clonal selection. According to the clonal selection theory, at birth, ... Affinity maturation Allelic exclusion Anergy Immune response Immune tolerance Immunosuppression Original antigenic sin Somatic ... Once activated, the CTL undergoes a process called clonal selection, in which it gains functions and divides rapidly to produce ... which builds on the existing clonal selection hypothesis and since 1974 has been developed mainly by Niels Jerne and Geoffrey W ...
Clonal+anergy at the U.S. National Library of Medicine Medical Subject Headings (MeSH) (Articles with short description, Short ... Jenkins MK (February 1992). "The role of cell division in the induction of clonal anergy". Immunology Today. 13 (2): 69-73. doi ... 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 ...
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 ...
Major histocompatibility complex independent clonal T cell anergy by direct interaction of Staphylococcus aureus enterotoxin B ...
B-lymphocytes receptors, antigen, B-cell, clonal anergy, signal transduction receptors, IgC. The primary goals of Dr. Cambiers ... B-lymphocytes, prediabetic state, autoimmunity, autoantibodies, clonal anergy. The main focus of Dr. Smiths research is in ... and pathways that normally function to maintain B cell anergy. The Cambier Laboratory is currently studying these mechanisms in ...
Proposed by Gustav Nossal, the "Clonal Anergy theory" suggests that reactive T- or B-cells become deactivated during ... The "Clonal Deletion theory," suggests that self-reactive lymphoid cells are eliminated during immunological development. ... Further theories currently being investigated include the "Clonal Ignorance theory," and the "Suppressor population or ... Regulatory T cell theory." The "Clonal Ignorance theory" suggests that self-reactive T cells not present in the thymus move to ...
Whereas clonal deletion and anergy are mechanisms of peripheral tolerance2,3, active suppression by T-regulatory 1 (Tr1) cells ... Whereas clonal deletion and anergy are mechanisms of peripheral tolerance2,3, active suppression by T-regulatory 1 (Tr1) cells ... Evidence for a thymus-dependent form of tolerance that is not based on elimination or anergy of reactive T cells. Immunol. Rev. ... Kappler, J. W., Roehm, N. & Marrack, P. T cell tolerance by clonal elimination in the thymus. Cell 49, 273-280 (1987) ...
Clonal anergy induced in mature Vβ6+ T lymphocytes on immunizing Mls-1b mice with Mls-1a expressing cells ... Clonal anergy induced in mature Vβ6+ T lymphocytes on immunizing Mls-1b mice with Mls-1a expressing cells ... It may be informative to compare CD4+ T cell anergy induced with anti-4-1BB mAbs with CD4+ T cell anergy induced by SAg 15,16. ... a minority of responding T cells survive a primary SAg stimulus with long-term anergy 15,16,17,18. Anergy is controlled by ...
Schwartz RH: A cell culture model for T lymphocyte clonal anergy. Science. 1990, 248 (4961): 1349-1356. 10.1126/science.2113314 ... T-cell anergy is defined as the state in which T-cells fail to respond to previously encountered antigenic stimulation by ... As the main ligand for PD-1, PD-L1 induces a co-inhibitory signal in activated T-cells and promotes T-cell apoptosis, anergy ...
Schwartz RH: T cell clonal anergy. Curr Opinion Immunol. 1997, 9: 351-357. 10.1016/S0952-7915(97)80081-7. ... Transactivation by AP-1 is a molecular target of T cell clonal anergy. Science. 1992, 257: 1134-1138. ... As the immune response proceeds over time, TNF is required to suppress subsequent clonal expansion (TNF+/+; unbroken line). In ... This therapeutic approach is in line with the thesis proposing that susceptibility to autoimmunity arises not through clonal ...
Circulating antibodies are produced by clonal B cells that specifically respond to only one antigen (an example is a virus ...
A cell culture model for T lymphocyte clonal anergy. Science 1990;248:1349-1356. ...
Reversion of anergy signatures in clonal CD21 low B cells of mixed cryoglobulinemia after clearance of HCV viremia ... Lck Is a Crucial Anergy Regulator in CLL Alexander Fuchs, Melanie Märklin, PhD, Jonas Heitmann, Felicia Truckenmüller, ... The phosphotyrosine phosphatase SHP2 promotes anergy in chronic lymphocytic leukemia Simon Schliffke, Sophia Buhs, Sarah Bolz, ...
This is called as Clonal Anergy. This is the functional inactivation of surviving self reacting T-cells. Proper signals are not ... Clonal deletion is the destruction of self-reactive T-cells in thymus. It is called as central tolerance. Tolerance acquired ...
Pike B, Boyd A, Nossal G (1982). "Clonal anergy: the universally anergic B lymphocyte". Proc Natl Acad Sci U S A. 79 (6): 2013- ... Clonal Anergy theory, proposed by Nossal, in which self-reactive T- or B-cells become inactivated in the normal individual and ... Clonal Deletion theory, proposed by Burnet, according to which self-reactive lymphoid cells are destroyed during the ... The so-called "Clonal Ignorance" theory, according to which host immune responses are directed to ignore self-antigens[4] ...
... the intrathymic clonal deletion associated with intrathymic chimerism, and the clonal anergy. The generation of suppressor T ... Those include the clonal destruction of antigen-stimulated mature T cells, the peripheral clonal deletion associated with ... produced through the clonal destruction mechanism. For this purpose, the tolerogen, antimitotic drugs, their doses, timing, ...
cell activity, clonal anergy, dendritic cell, lymphocyte proliferation, interleukin 2 receptor, T lymphocyte ...
Clonal anergy. *Clonal deletion. *Tolerance in pregnancy. *Immunodeficiency. Immunogenetics. *Affinity maturation *Somatic ...
Clonal anergy. *Clonal deletion. *Tolerance in pregnancy. *Immunodeficiency. Immunogenetics. *Affinity maturation *Somatic ...
This results in the cell becoming anergic (anergy is generated from the unprotected biochemical changes of Signal 1). Anergic ...
N2 - The mechanisms for achieving self/non-self distinction include clonal deletion, clonal anergy, and clonal balance. Clonal ... AB - The mechanisms for achieving self/non-self distinction include clonal deletion, clonal anergy, and clonal balance. Clonal ... The mechanisms for achieving self/non-self distinction include clonal deletion, clonal anergy, and clonal balance. Clonal ... These self-reactive T cells are normally held in check by clonal anergy or clonal balance. Anergy occurs when a T cell receives ...
Pathways for this include an unresponsive state known as anergy, clonal deletion, and T regulatory (Treg) cell induction. The ... Tolerized BATF-deficient CD4+ T cells were resistant to anergy induction and instead underwent clonal deletion due to ... Anergia Clonal , Fator de Transcrição AP-1 , Proteína 11 Semelhante a Bcl-2/genética , Linfócitos T Reguladores , Autoantígenos ... The data identify the AP-1 nuclear factor BATF as a dominant driver of sustained T cell anergy and illustrate a mechanism for ...
... autoimmune reactions are avoided because of the immunologic tolerance mechanisms of clonal deletion and clonal anergy. Any ...
Clonal anergy induced in mature Vß6+ T lymphocytes on immunizing Mls-1b mice with Mls-1a expressing cells. Nature 339:541-544. ... induction of T cell anergy in vivo (Nature 1989; 339: 541; 542 citations), 6) used a covalent peptide/TLR-ligand compound for ...
Clonal anergy induced in mature Vß6+ T lymphocytes on immunizing Mls-1b mice with Mls-1a expressing cells. Nature 339:541-544. ... induction of T cell anergy in vivo (Nature 1989; 339: 541; 542 citations), 6) used a covalent peptide/TLR-ligand compound for ...
Attempts to restore natural immunotolerance by causing clonal anergy and/or deletion of autoreactive T-cells, have been ...
Powell, J.D.; Lerner, C.G.; Schwartz, R.H. Inhibition of cell cycle progression by rapamycin induces T cell clonal anergy even ... Antagonistic roles for CTLA-4 and the mammalian target of rapamycin in the regulation of clonal anergy: Enhanced cell cycle ... mTOR inhibitors have been shown to have a significant role in promoting T-cell anergy both in vitro [64] and in vivo studies [ ...
The data presented indicate that activation, clonal expansion, anergy, and death of V beta 8.3+ T cells occur sequentially ...
The escape of anti-self B cells from tolerance mechanisms like clonal deletion, receptor editing, and anergy results in the ... The results highlight the prominence of early childhood B cell clonal expansions and cross-reactivity for future responses to ... Vaccination and infection promote the formation, tissue distribution, and clonal evolution of B cells, which encode humoral ...
  • There is also accumulating evidence that beside clonal deletion and anergy, regulatory T cells−mediated dominant control of self−reactive lymphocytes might contribute to the maintenance of immunologic self−tolerance. (lu.se)
  • This phenomenon was first described in B lymphocytes by Gustav Nossal and termed "clonal anergy. (wikipedia.org)
  • Proposed by Gustav Nossal, the "Clonal Anergy theory" suggests that reactive T- or B-cells become deactivated during development and fail to increase immune responses. (news-medical.net)
  • The "Clonal Deletion theory," suggests that self-reactive lymphoid cells are eliminated during immunological development. (news-medical.net)
  • The "Clonal Ignorance theory" suggests that self-reactive T cells not present in the thymus move to the periphery where they fail to encounter target antigens . (news-medical.net)
  • Evidence for a thymus-dependent form of tolerance that is not based on elimination or anergy of reactive T cells. (nature.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. (wikidoc.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. (wikidoc.org)
  • Clonal deletion results in the elimination of self-reactive T cells during their maturation in the thymus. (johnshopkins.edu)
  • T cells reactive with self-antigens not represented in the thymus, and probably some low-affinity T cells, escape clonal deletion and populate peripheral lymphoid tissues and blood. (johnshopkins.edu)
  • These self-reactive T cells are normally held in check by clonal anergy or clonal balance. (johnshopkins.edu)
  • METHODS: We used immobilized anti-CD3 monoclonal antibody (mAb) to induce anergy in T helper (Th) 1 and Th0 cells reactive with MHC class II molecule H2 I-Ab. (ox.ac.uk)
  • In immunology, anergy is 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)
  • Pathways for this include an unresponsive state known as anergy, clonal deletion, and T regulatory (Treg) cell induction. (bvsalud.org)
  • Tolerized BATF-deficient CD4+ T cells were resistant to anergy induction and instead underwent clonal deletion due to proapoptotic BIM (Bcl2l11) upregulation. (bvsalud.org)
  • We previously proven that carrying out a incomplete reconstitution from the Compact disc4+ T cell area in lymphopenic hosts Compact disc25+ Foxp3+ Compact disc4+ T regulatory cells play a significant role to advertise Ag-specific tolerance within Compact disc4+ T cells through the induction of clonal anergy. (hiv-proteases.com)
  • BACKGROUND: In this study, we have investigated the mechanisms involved in both the induction of suppressive anergy, the stability of the anergy induced, and the possible mechanisms by which the response of immunocompetent CD4+ T cells are suppressed. (ox.ac.uk)
  • 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)
  • In Cabozantinib FLt inhibitor the peripheral immune protection system the important thing systems that induce and sustain tolerance include clonal removal, anergy, prejudice, and withdrawal. (hdacassay.com)
  • Special care was taken to overcome the " hard" barriers of allo- or xeno-combinations by reducing the "split tolerance" produced through the clonal destruction mechanism. (nih.gov)
  • The data identify the AP-1 nuclear factor BATF as a dominant driver of sustained T cell anergy and illustrate a mechanism for divergent peripheral tolerance fates. (bvsalud.org)
  • In this review we summarize our findings using a TCR-γδ transgenic model where self-tolerance was maintained by clonal deletion for cells localizing to peripheral lymphold tissue and by clonal anergy for cells localizing to the intraepithelial compartments. (uky.edu)
  • Further theories currently being investigated include the "Clonal Ignorance theory," and the "Suppressor population or Regulatory T cell theory. (news-medical.net)
  • Clinical investigations have reported abnormal cellular immunity with anergy to recall antigens or an imbalance between helper T- and suppressor T-cells. (biomedcentral.com)
  • In this case NFAT homodimerizes (complexes with itself), working as a transcriptional factor that induces anergy in the lymphocyte instead. (wikipedia.org)
  • The clonal expansion of those cells can lead to autoimmune diseases, wherein the body attacks itself. (wikipedia.org)
  • The mechanisms for achieving self/non-self distinction include clonal deletion, clonal anergy, and clonal balance. (johnshopkins.edu)
  • T-cell anergy is defined as the state in which T-cells fail to respond to previously encountered antigenic stimulation by functional APCs. (biomedcentral.com)
  • Those include the clonal destruction of antigen-stimulated mature T cells, the peripheral clonal deletion associated with peripheral chimerism, the intrathymic clonal deletion associated with intrathymic chimerism, and the clonal anergy. (nih.gov)
  • Clonal balance depends upon the ratio of stimulatory and inhibitory signals delivered to the T cells. (johnshopkins.edu)
  • The data presented indicate that activation, clonal expansion, anergy, and death of V beta 8.3+ T cells occur sequentially after UDA administration. (aai.org)
  • RESULTS: We observed that suppressive anergy was induced independently of costimulation in Th0 but not Th1 cells. (ox.ac.uk)
  • Neither anergy nor suppression was observed in Th0 cells upon restimulation with anti-CD3 in the presence of syngeneic antigen-presenting cells (APCs). (ox.ac.uk)
  • However, anergy but not suppression was observed in co-cultures restimulated with anti-T-cell antigen receptor (TCR) mAbs/syngeneic APCs and suppression could be restored by the addition of I-Ab+ APCs. (ox.ac.uk)
  • At the cellular level, "anergy" is the inability of an immune cell to mount a complete response against its target. (wikipedia.org)
  • A Novel, Heterozygous Three Base-Pair Deletion in CARD11 Results in B Cell Expansion with NF-κB and T Cell Anergy Disease. (ox.ac.uk)
  • Anergy occurs when a T cell receives its antigen-specific signal in the absence of required co-stimulatory signals. (johnshopkins.edu)
  • 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)
  • Germline gain-of-function mutations in CARD11 lead to the primary immunodeficiency, B cell expansion with NF-κB, and T cell anergy (BENTA). (ox.ac.uk)
  • This process - called "clonal expansion" - allows the body to quickly mobilise an army of clones, as and when required. (wikipedia.org)
  • This specific clonal army then combats the pathogen until the body is free of the infection. (wikipedia.org)
  • 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)
  • Tolerance can be categorized into three types: (1) clonal deletion (central tolerance), (2) clonal anergy (peripheral tolerance), and (3) active cellular suppressive mechanisms. (nih.gov)
  • The most stable type of tolerance is clonal deletion, whereby specific reactive T cells (i.e. (nih.gov)
  • Tolerance may be induced by a variety of approaches, including: clonal deletion, clonal anergy, immune deviation, or suppression. (nih.gov)
  • Normally, potentially pathologic autoimmune reactions are avoided because of the immunologic tolerance mechanisms of clonal deletion and clonal anergy. (merckmanuals.com)
  • Clonal deletion induced by either radioresistant thymic host cells or lymphohemopoietic donor cells at different stages of class I-restricted T cell ontogeny. (rupress.org)
  • However, radioresistant components of the thymus also influence negative selection, but it remains controversial whether this is accomplished by clonal deletion, clonal anergy, or other mechanisms. (rupress.org)
  • In contrast, chimeras expressing H-2Db on lymphohemopoietic donor cells showed clonal deletion at a later stage during ontogeny. (rupress.org)
  • There are several types of tolerance including: clonal deletion, anergy, suppression, and immunological ignorance (lack of sufficient antigen to achieve levels of receptor binding required for signaling). (umn.edu)
  • There is also accumulating evidence that beside clonal deletion and anergy, regulatory T cells−mediated dominant control of self−reactive lymphocytes might contribute to the maintenance of immunologic self−tolerance. (lu.se)
  • Immunological tolerance which is primarily mediated by the clonal deletion of autoreactive T cells in the thymus is a key feature of the immune system. (hu-berlin.de)
  • 9. 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)
  • Induction of anergy is one means by which tolerance to antigens in peripheral tissues is induced, thus avoiding an autoimmune response [ 26 ]. (biomedcentral.com)
  • In immunology, anergy is 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)
  • Early growth response gene-2, a zinc-finger transcription factor, is required for full induction of clonal anergy in CD4+ T cells. (umassmed.edu)
  • These findings suggested that the anergy of B cells in congenitally infected chickens is caused by the developmental arrest and dysfunction of B cell progenitors, which is an important factor for the immunological tolerance induced by ALV-J. (biomedcentral.com)
  • Experimental data collected in animal models and humans have also shown that the B cell anergy induced by hepatitis B virus (HBV) and human immunodeficiency virus (HIV) can cause immunological tolerance, especially in the context of congenital infection [ 18 , 19 ]. (biomedcentral.com)
  • Our results show a critical role for Cbl-b in the regulation of peripheral tolerance and anergy of T cells. (nih.gov)
  • This phenomenon was first described in B lymphocytes by Gustav Nossal and termed "clonal anergy. (wikipedia.org)
  • Depletion of the programmed death-1 receptor completely reverses established clonal anergy in CD4(+) T lymphocytes via an interleukin-2-dependent mechanism. (umassmed.edu)
  • In this case NFAT homodimerizes (complexes with itself), working as a transcriptional factor that induces anergy in the lymphocyte instead. (wikipedia.org)
  • Receptor-independent stimulation of Tgfb1(-/-) T cells by PMA plus ionomycin induces IL-2 production and mitogenic response, and it rescues them from anergy. (nih.gov)
  • NFAT homodimers are directly responsible for the expression of anergy associated genes such as ubiquitin ligase GRAIL or a protease caspase 3. (wikipedia.org)
  • We also observed strong positive correlation between differentially expressed epigenetic regulatory genes and degree of clonal expansion, suggesting epigenetic regulation may be involved in B cell anergy. (nih.gov)
  • 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)
  • At the cellular level, "anergy" is the inability of an immune cell to mount a complete response against its target. (wikipedia.org)
  • In some infections, such as human cytomegalovirus , there is a clonal expansion of peripheral γδ T cells that have specific TCRs, indicating the adaptive nature of the immune response mediated by these cells. (relationship983.cfd)
  • In peripheral B cells from HCV-associated BNHL patients, we observed enrichment of a transcriptional signature associated with B cell anergy. (nih.gov)
  • A beta-gal-specific CD4 T cell receptor transgenic mouse has been made to provide a clonal population of naive T cells with specificity for this antigen. (umn.edu)
  • 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)
  • This clone has been further utilized as a model for studying T cell clonal anergy. (nih.gov)
  • Viral tropism was determined by PCR and sequencing, applying the clonal and clinical model of analyses. (beds.ac.uk)