Homeostatic inflammation in innate immunity.
Homeostatic inflammation in innate immunity.
复制标题
先天免疫中的稳态炎症。
DOI：
10.1016/j.coi.2014.08.003
复制
发表时间：
2014
期刊：
影响因子：
--
通讯作者：
T. Kaisho
中科院分区：
文献类型：
--
作者：
K. Miyake;T. Kaisho
亮点病原体感应器不仅对病原体有反应，而且对自身衍生的产物也有反应。自身衍生的产物是代谢产物，如脂肪酸或核酸。代谢产物激活感受器，导致动态平衡炎症。内分泌体是动态平衡炎症的重要细胞内平台。树突状细胞以亚群特异性的方式导致动态平衡炎症。先天免疫感应器不仅对微生物产物，而且对内源性代谢物，如核酸(NAS)和脂类作出反应。Toll样受体(TLRs)从质膜和内溶酶体传递信号，在内溶酶体中Nas和脂质被分解。TLRs与内溶酶体中的代谢产物相互作用导致动态平衡的TLR激活。表达NA敏感TLRs的树突状细胞被宿主或共生体的代谢物稳定地激活，并产生I型IFN，从而引发各种类型的炎症条件。在这里，我们讨论动态平衡炎症是如何由先天免疫感受器诱导的，并参与维持免疫动态平衡和引起非传染性炎症性疾病。
HighlightsPathogen sensors respond not only to pathogens but also to self-derived products.The self-derived products are metabolites such as fatty acids or nucleic acids.The metabolites activate sensors to lead to the homeostatic inflammation.Endolysosome is a crucial intracellular platform for the homeostatic inflammation.Dendritic cells lead to the homeostatic inflammation in a subset-specific way.Innate immune sensors respond not only to microbial products but also to endogenous metabolites such as nucleic acids (NAs) and lipids. Toll-like receptors (TLRs) deliver a signal from the plasma membrane and also from endolysosomes, where NAs and lipids are catabolized. Interaction of TLRs with metabolites in endolysosomes leads to homeostatic TLR activation. Dendritic cells expressing NA-sensing TLRs are steadily activated by metabolites derived from the host or commensals and produce type I IFNs, thereby provoking various types of inflammatory conditions. Here, we discuss how homeostatic inflammation is induced by innate immune sensors and is involved in maintaining immune homeostasis and causing non-infectious inflammatory diseases.