Recurrent superantigen exposure <i>in vivo</i> leads to highly suppressive CD4+CD25+ and CD4+CD25- T cells with anergic and suppressive genetic signatures

Schartner, Jill; Singh, Anju; Dahlberg, P.E.; Nettenstrom, Lauren; Seroogy, Christine M.

doi:10.1111/j.1365-2249.2008.03827.x

Cited by 18 publications

(15 citation statements)

References 22 publications

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“…Thus, balance between varied isoforms of otubain‐1 in T cells determines GRAIL level and therefore the outcome of antigenic challenge. Furthermore, recent studies have proposed that GRAIL targets and ubiquitinates transmembrane proteins such as CD40, CD151, and CD81 (85, 86).…”

Section: Signaling Basis Of T‐cell Tolerancementioning

confidence: 99%

Molecular mechanisms of T‐cell tolerance

Nurieva

Liu

Dong

2011

Immunological Reviews

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Summary CD4+ T cells are the master regulators of adaptive immune responses, and many autoimmune diseases arise due to a breakdown of self-tolerance in CD4+ T cells. Activation of CD4+ T cells is regulated by not only the binding of peptide-major histocompatibility complexes to T-cell receptor but also costimulatory signals from antigen-presenting cells. Recently, there has been progress in understanding the extracellular and intracellular mechanisms that are required for implementation and maintenance of T-cell tolerance. Understanding of the molecular mechanisms underlying T-cell tolerance will lead to development of pharmacological approaches either to promote the tolerance state in terms of autoimmunity or to break tolerance in cancer.

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Section: Signaling Basis Of T‐cell Tolerancementioning

confidence: 99%

Molecular mechanisms of T‐cell tolerance

Nurieva

Liu

Dong

2011

Immunological Reviews

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“…In addition to toxin-specific resistance elicited by a single oral dose of SE, chronic intravenous exposure to SEA can delete Vβ-reactive T cells in mice 89 . This may be partly explained by increased frequency of FoxP3 + CD4 + regulatory T cells observed in TCR transgenic mice repeatedly exposed to SEB 90 .…”

Section: In Vivo Effects: Animal Models and Morementioning

confidence: 99%

The staphylococcal enterotoxin (SE) family

Krakauer

Stiles

2013

Virulence

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Staphylococcus aureus plays an important role in numerous human cases of food poisoning, soft tissue, and bone infections, as well as potentially lethal toxic shock. This common bacterium synthesizes various virulence factors that include staphylococcal enterotoxins (SEs). These protein toxins bind directly to major histocompatibility complex class II on antigen-presenting cells and specific Vβ regions of T-cell receptors, resulting in potentially life-threatening stimulation of the immune system. Picomolar concentrations of SEs ultimately elicit proinflammatory cytokines that can induce fever, hypotension, multi-organ failure, and lethal shock. Various in vitro and in vivo models have provided important tools for studying the biological effects of, as well as potential vaccines/therapeutics against, the SEs. This review succinctly presents known physical and biological properties of the SEs, including various intervention strategies. In particular, SEB will often be portrayed as per biodefense concerns dating back to the 1960s.

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“…RhoGDI has been identified as a potential substrate for GRAIL, suggesting a role for the Rho signaling pathway in establishing anergy phenotype in T cells [214]. In addition, recent studies have identified potential targets of GRAIL, such as CD40, CD151 and CD81 [215,216]. …”

Section: Molecular Mechanisms Of T-cell Tolerancementioning

confidence: 99%

T-Cell Tolerance in Cancer

2013

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T cells are the master regulators of adaptive immune responses and maintenance of their tolerance is critical to prevent autoimmunity. However, in the case of carcinogenesis, the tumor microenvironment aids T-cell tolerance, which contributes to uncontrolled tumor growth. Recently, there has been significant progress in understanding the intrinsic extracellular (positive and negative costimulatory molecules on APCs) and intracellular mechanisms (E3 ubiquitin ligases, transcriptional and epigenetic repressors), as well as extrinsic mechanisms (Tregs and tolerogenic dendritic cells) that are required for the implementation and maintenance of T-cell tolerance. Ultimately, understanding and manipulating T-cell tolerance will help to break the tolerance state in cancer.

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Recurrent superantigen exposure in vivo leads to highly suppressive CD4+CD25+ and CD4+CD25- T cells with anergic and suppressive genetic signatures

Cited by 18 publications

References 22 publications

Molecular mechanisms of T‐cell tolerance

Molecular mechanisms of T‐cell tolerance

The staphylococcal enterotoxin (SE) family

T-Cell Tolerance in Cancer

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