Autophagy in infection, inflammation and immunity.
Autophagy in infection, inflammation and immunity.
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DOI：
10.1038/nri3532
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发表时间：
2013-10
期刊：
影响因子：
--
通讯作者：
Akira S
中科院分区：
文献类型：
--
作者：
Deretic V;Saitoh T;Akira S
自噬是影响免疫的基本细胞生物学途径。自噬是常规模式识别受体（PRR）的抗微生物效应子，而称为SLR的自噬衔接子代表PRR的新子集，并为细胞内微生物的自噬消除提供机制基础。自噬通过与先天免疫信号传导的调节相互作用，通过去除内源性炎性体激动剂以及对免疫介质分泌的彻底影响来控制炎症。自噬有助于抗原呈递，T细胞稳态，并影响T细胞库和极化，包括Th17炎症。在这里，我们回顾了自噬在感染、炎症和免疫中的四个主要作用。
Autophagy is a fundamental cell biological pathway affecting immunity. Whereas autophagy is an antimicrobial effector of conventional pattern recognition receptors (PRRs), autophagic adaptors termed SLRs represent a new subset of PRRs and provide the mechanistic basis for autophagic elimination of intracellular microbes. Autophagy controls inflammation via regulatory interactions with innate immunity signalling, by removing endogenous inflammasome agonists, and thorough effects on secretion of immune mediators. Autophagy contributes to antigen presentation, T cell homeostasis, and affects T cell repertories and polarization including Th17 inflammation. Here, we review the above relationships organized into four principal roles of autophagy in infection, inflammation, and immunity.