Cytosolic DNA sensors regulating type I interferon induction

被引：229

作者：

Keating, Sinead E. ^{[1
]}

Baran, Marcin ^{[1
,2
]}

Bowie, Andrew G. ^{[1
,2
]}

机构：

[1] Trinity Coll Dublin, Sch Biochem & Immunol, Dublin 2, Ireland

[2] Trinity Coll Dublin, Immunol Res Ctr, Dublin 2, Ireland

来源：

TRENDS IN IMMUNOLOGY | 2011年 / 32卷 / 12期

基金：

爱尔兰科学基金会;

关键词：

SYSTEMIC-LUPUS-ERYTHEMATOSUS; PLASMACYTOID DENDRITIC CELLS; INNATE IMMUNE-RESPONSE; PRIMARY SJOGRENS-SYNDROME; NF-KAPPA-B; TLR9-INDEPENDENT PATHWAYS; FRANCISELLA-TULARENSIS; AIM2; INFLAMMASOME; INTRACELLULAR DNA; HIN-200; FAMILY;

D O I：

10.1016/j.it.2011.08.004

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

071005 [微生物学]; 100108 [医学免疫学];

摘要：

Type I interferon (IFN) induction is a crucial anti-pathogen response mediated by innate immune stimulation. Although it has been appreciated for some time that the presence of pathogen DNA within a cell leads to a type I IFN response, it is only in the past few years that some of the key signalling proteins and DNA sensors that regulate this response have been uncovered. Here, we review the nature of these DNA sensors, which include a new family of pattern recognition receptors termed the AIM2-like receptors, and consider the implications of their discovery for understanding emerging principles of innate immune DNA sensing. Furthermore, we discuss how their discovery provides a rationale as to why accumulation of self-DNA mediates IFN-dependent autoimmunity.

引用

页码：574 / 581

页数：8

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