AIRE expands: new roles in immune tolerance and beyond

被引:164
作者
Anderson, Mark S. [1 ]
Su, Maureen A. [2 ,3 ,4 ]
机构
[1] Univ Calif San Francisco, Ctr Diabet, San Francisco, CA 94143 USA
[2] Univ N Carolina, Sch Med, Dept Pediat, Chapel Hill, NC 27599 USA
[3] Univ N Carolina, Sch Med, Dept Microbiol & Immunol, Chapel Hill, NC 27599 USA
[4] Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA
关键词
THYMIC EPITHELIAL-CELLS; REGULATORY T-CELLS; PROMISCUOUS GENE-EXPRESSION; TISSUE-RESTRICTED ANTIGENS; AUTOIMMUNE REGULATOR; SELF-ANTIGEN; IMMUNOLOGICAL-TOLERANCE; P-TEFB; DIFFERENTIATION PROGRAM; ECTOPIC EXPRESSION;
D O I
10.1038/nri.2016.9
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
More than 15 years ago, mutations in the autoimmune regulator (AIRE) gene were identified as the cause of autoimmune polyglandular syndrome type 1 (APS1). It is now clear that this transcription factor has a crucial role in promoting self-tolerance in the thymus by regulating the expression of a wide array of self-antigens that have the commonality of being tissue-restricted in their expression pattern in the periphery. In this Review, we highlight many of the recent advances in our understanding of the complex biology that is related to AIRE, with a particular focus on advances in genetics, molecular interactions and the effect of AIRE on thymic selection of regulatory T cells. Furthermore, we highlight new areas of biology that are potentially affected by this key regulator of immune tolerance.
引用
收藏
页码:247 / 258
页数:12
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