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We are analyzing https://www.nature.com/articles/s41577-020-00454-2.

Title:
Rethinking peripheral T cell tolerance: checkpoints across a T cell’s journey | Nature Reviews Immunology
Description:
Following their exit from the thymus, T cells are endowed with potent effector functions but must spare host tissue from harm. The fate of these cells is dictated by a series of checkpoints that regulate the quality and magnitude of T cell-mediated immunity, known as tolerance checkpoints. 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. At the naive T cell stage, two intrinsic checkpoints that actively maintain tolerance are quiescence and ignorance. In the presence of co-stimulation-deficient T cell activation, anergy is a dominant hallmark that mandates T cell unresponsiveness. When T cells are successfully stimulated and reach the effector stage, exhaustion and senescence can limit excessive inflammation and prevent immunopathology. At every stage of the T cell’s journey, cell death exists as a checkpoint to limit clonal expansion and to terminate unrestrained responses. Here, we compare and contrast the T cell tolerance checkpoints and discuss their specific roles, with the aim of providing an integrated view of T cell peripheral tolerance and fate regulation. A number of T cell-intrinsic peripheral tolerance mechanisms (quiescence, ignorance, anergy, exhaustion, senescence and cell death) restrain autoimmunity and overactive immune responses. Here, the authors provide an integrated perspective of peripheral T cell tolerance by comparing the molecular mechanisms that govern these checkpoints and discussing their role in T cell tolerance and fate regulation.
Website Age:
30 years and 10 months (reg. 1994-08-11).

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Keywords {🔍}

pubmed, google, scholar, cas, cell, cells, central, immunol, nature, nat, immunity, tolerance, exhaustion, med, anergy, infection, exp, article, rev, quiescence, human, death, induction, viral, peripheral, immune, expression, tcell, function, activation, memory, vivo, anergic, cancer, immunology, senescence, naive, access, factor, transcription, receptor, tumor, science, differentiation, sci, chronic, role, autoimmunity, gene, content,

Topics {✒️}

permissions reprints privacy policy nature portfolio journals class i-restricted cross-presentation nature portfolio advertising hla-drb10401-positive humanized mice highly differentiated cd8+cd28-cd27 author information authors social media tis21/pc3/btg1/tob family human cd4+cd45ra+cd27- memory jun nh2-terminal kinase c-myc-dependent pathway antigen-specific t-cell anergy immunodominant epstein-barr virus multifunctional cd4+cd45ra+cd27+ zinc-finger transcription factor author correspondence tumor-draining lymph node varicella-zoster virus antigen kinase p38 activated programmed death-1hi cd8 cross-tolerizing endogenous antigen restimulation-induced cell death inducing t-cell tolerance personal data virus-specific memory cd8+ prolonged interleukin-2ralpha expression multi-lineage immune checkpoint bcl-2-inhibitable pathway mediated cd4 t-lymphocyte unresponsiveness kinase signaling pathways activation-induced cell death nature https inhibitory b7-family molecules data protection permissions antigen-independent memory cd8 restore anti-tumor immunity peripheral t-cell tolerance springerlink instant access diacylglycerol kinase-alpha regulatory tumor-specific cd4+ cell receptor signaling il-2-regulated fas-mediated soluble viral peptides reactive oxygen species crucial dysfunctional states long-lived memory cells

Questions {❓}

  • How does an anti-CTLA-4 antibody promote cancer immunity?
  • Immunity and immunopathology to viruses: what decides the outcome?
  • Precursor exhausted T cells: key to successful immunotherapy?
  • Will telomere erosion lead to a loss of T-cell memory?

Schema {🗺️}

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      headline:Rethinking peripheral T cell tolerance: checkpoints across a T cell’s journey
      description:Following their exit from the thymus, T cells are endowed with potent effector functions but must spare host tissue from harm. The fate of these cells is dictated by a series of checkpoints that regulate the quality and magnitude of T cell-mediated immunity, known as tolerance checkpoints. 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. At the naive T cell stage, two intrinsic checkpoints that actively maintain tolerance are quiescence and ignorance. In the presence of co-stimulation-deficient T cell activation, anergy is a dominant hallmark that mandates T cell unresponsiveness. When T cells are successfully stimulated and reach the effector stage, exhaustion and senescence can limit excessive inflammation and prevent immunopathology. At every stage of the T cell’s journey, cell death exists as a checkpoint to limit clonal expansion and to terminate unrestrained responses. Here, we compare and contrast the T cell tolerance checkpoints and discuss their specific roles, with the aim of providing an integrated view of T cell peripheral tolerance and fate regulation. A number of T cell-intrinsic peripheral tolerance mechanisms (quiescence, ignorance, anergy, exhaustion, senescence and cell death) restrain autoimmunity and overactive immune responses. Here, the authors provide an integrated perspective of peripheral T cell tolerance by comparing the molecular mechanisms that govern these checkpoints and discussing their role in T cell tolerance and fate regulation.
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