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本文引用的文献

1
The E3 ubiquitin ligase GRAIL regulates T cell tolerance and regulatory T cell function by mediating T cell receptor-CD3 degradation.E3 泛素连接酶 GRAIL 通过介导 T 细胞受体-CD3 的降解来调节 T 细胞耐受和调节性 T 细胞功能。
Immunity. 2010 May 28;32(5):670-80. doi: 10.1016/j.immuni.2010.05.002. Epub 2010 May 20.
2
Metabolism in T cell activation and differentiation.T 细胞活化和分化中的代谢。
Curr Opin Immunol. 2010 Jun;22(3):314-20. doi: 10.1016/j.coi.2010.01.018. Epub 2010 Feb 26.
3
Dual function of CTLA-4 in regulatory T cells and conventional T cells to prevent multiorgan autoimmunity.CTLA-4 在调节性 T 细胞和常规 T 细胞中的双重功能,以预防多器官自身免疫。
Proc Natl Acad Sci U S A. 2010 Jan 26;107(4):1524-8. doi: 10.1073/pnas.0910341107. Epub 2010 Jan 4.
4
Role of conserved non-coding DNA elements in the Foxp3 gene in regulatory T-cell fate.调控性 T 细胞命运中 Foxp3 基因中保守非编码 DNA 元件的作用。
Nature. 2010 Feb 11;463(7282):808-12. doi: 10.1038/nature08750. Epub 2010 Jan 13.
5
Skin-draining lymph nodes contain dermis-derived CD103(-) dendritic cells that constitutively produce retinoic acid and induce Foxp3(+) regulatory T cells.皮肤引流淋巴结包含真皮衍生的 CD103(-)树突状细胞,这些细胞持续产生视黄酸并诱导 Foxp3(+)调节性 T 细胞。
Blood. 2010 Mar 11;115(10):1958-68. doi: 10.1182/blood-2009-09-245274. Epub 2010 Jan 12.
6
CTLA-4 suppresses the pathogenicity of self antigen-specific T cells by cell-intrinsic and cell-extrinsic mechanisms.CTLA-4 通过细胞内和细胞外机制抑制自身抗原特异性 T 细胞的致病性。
Nat Immunol. 2010 Feb;11(2):129-35. doi: 10.1038/ni.1835. Epub 2009 Dec 27.
7
Anergic T cells are metabolically anergic.无反应性T细胞在代谢上呈无反应性。
J Immunol. 2009 Nov 15;183(10):6095-101. doi: 10.4049/jimmunol.0803510. Epub 2009 Oct 19.
8
Retinoic acid can enhance conversion of naive into regulatory T cells independently of secreted cytokines.视黄酸可独立于分泌的细胞因子增强天然T细胞向调节性T细胞的转化。
J Exp Med. 2009 Sep 28;206(10):2131-9. doi: 10.1084/jem.20090639. Epub 2009 Sep 8.
9
Deltex1 is a target of the transcription factor NFAT that promotes T cell anergy.Deltex1是促进T细胞无反应性的转录因子NFAT的一个靶点。
Immunity. 2009 Jul 17;31(1):72-83. doi: 10.1016/j.immuni.2009.04.017.
10
Infectious tolerance via the consumption of essential amino acids and mTOR signaling.通过必需氨基酸消耗和mTOR信号传导实现的感染性耐受。
Proc Natl Acad Sci U S A. 2009 Jul 21;106(29):12055-60. doi: 10.1073/pnas.0903919106. Epub 2009 Jun 30.

诱导 T 细胞失能:环境线索与感染性耐受的整合。

Induction of T cell anergy: integration of environmental cues and infectious tolerance.

机构信息

Laboratory of Cellular and Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.

出版信息

Curr Opin Immunol. 2010 Oct;22(5):552-9. doi: 10.1016/j.coi.2010.08.005. Epub 2010 Sep 24.

DOI:10.1016/j.coi.2010.08.005
PMID:20869863
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2981408/
Abstract

Anergy is a state of long-term hyporesponsiveness in T cells that is characterized by an active repression of TCR signaling and IL-2 expression [1]. Several forms of anergy have been described and the past few years have brought to light an increasing number of 'anergic factors' involved in the induction and the active maintenance of the state in lymphocytes. The role of mTOR and other related metabolic sensors and regulators has recently emerged as of particular importance in broadening our view of anergy-inducing signals. We will discuss the role of these molecules in regulating the choice between anergy and activation, a decision faced by all T cells undergoing TCR stimulation. We will then explore the relationship between the induction of anergy and the induction of regulatory T cells as well as the potential crosstalk responsible for the phenomenon of infectious tolerance.

摘要

失能是 T 细胞长期低反应状态的一种表现,其特征为 TCR 信号和 IL-2 表达受到主动抑制[1]。已描述了几种形式的失能,并且过去几年中,越来越多的“失能因子”被揭示参与了淋巴细胞中该状态的诱导和主动维持。mTOR 和其他相关代谢传感器和调节剂的作用最近在拓宽我们对诱导失能信号的认识方面显得尤为重要。我们将讨论这些分子在调节失能和激活之间的选择中的作用,所有经历 TCR 刺激的 T 细胞都面临着这一决策。然后,我们将探讨失能的诱导与调节性 T 细胞的诱导之间的关系,以及负责感染性耐受现象的潜在串扰。