Nucleic acid-sensing TLRs as modifiers of autoimmunity

被引:56
作者
Deane, Jonathan A. [1 ]
Bolland, Silvia [1 ]
机构
[1] NIAID, Immunogenet Lab, Rockville, MD 20852 USA
关键词
D O I
10.4049/jimmunol.177.10.6573
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The immune system requires precise regulation of activating and inhibitory signals so that it can mount effective responses against pathogens while ensuring tolerance to self-components. Some of the most potent activation signals are triggered by innate immune molecules, particularly those in the TLR family. Recent studies have shown that engagement of TLRs plays a significant role in both innate and adaptive immunity. This review focuses on the ways that TLR function might contribute to the etiology of lupus-like syndromes in the context of an autoimmune-prone environment. By considering the sources, localization, and expression of both nucleic acids and the molecules that bind them, we discuss several ways that innate immunity can play a role in the development of systemic autoimmunity.
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收藏
页码:6573 / 6578
页数:6
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