Host defense mechanisms triggered by microbial lipoproteins through toll-like receptors
Host defense mechanisms triggered by microbial lipoproteins through toll-like receptors
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DOI：
10.1126/science.285.5428.732
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发表时间：
1999-07-30
期刊：
影响因子：
56.9
通讯作者：
Modlin, RL
中科院分区：
文献类型：
--
作者：
Brightbill, HD;Libraty, DH;Modlin, RL
针对许多感染性病原体的细胞介导的免疫的产生涉及白细胞介素-12（IL-12）的产生，白细胞介素-12（IL-12）是先天免疫系统的关键信号。然而，对于许多病原体，诱导巨噬细胞产生IL-12的分子及其机制仍然不确定。在这里，它表明，微生物脂蛋白是人巨噬细胞产生IL-12的有效刺激剂，并且诱导由Toll样受体（TLR）介导。几种脂蛋白刺激TLR依赖的诱导型一氧化氮合酶的转录和一氧化氮的产生，这是一种强大的杀微生物途径。微生物脂蛋白激活TLR可能启动针对感染性病原体的先天防御机制。
The generation of cell-mediated immunity against many infectious pathogens involves the production of interleukin-12 (IL-12), a key signal of the innate immune system. Yet, for many pathogens, the molecules that induce IL-12 production by macrophages and the mechanisms by which they do so remain undefined. Here it is shown that microbial lipoproteins are potent stimulators of IL-12 production by human macrophages, and that induction is mediated by Toll-like receptors (TLRs). Several lipoproteins stimulated TLR-dependent transcription of inducible nitric oxide synthase and the production of nitric oxide, a powerful microbicidal pathway. Activation of TLRs by microbial lipoproteins may initiate innate defense mechanisms against infectious pathogens.