Cell activation and apoptosis by bacterial lipoproteins through toll-like receptor-2
Cell activation and apoptosis by bacterial lipoproteins through toll-like receptor-2
复制标题
DOI：
10.1126/science.285.5428.736
复制
发表时间：
1999-07-30
期刊：
影响因子：
56.9
通讯作者：
Zychlinsky, A
中科院分区：
文献类型：
--
作者：
Aliprantis, AO;Yang, RB;Zychlinsky, A
细胞凋亡与细菌病原体引起的炎症反应的产生和消退有关。所有细菌病原体产生脂蛋白（BLP），其触发先天免疫应答。发现BLP通过人Toll样受体2（hTLR 2）诱导THP-1单核细胞凋亡。BLP还在用hTLR 2转染的上皮细胞系中引发凋亡。此外，BLP刺激核因子-κ B，多个宿主防御基因的转录激活因子，并通过hTLR 2激活呼吸爆发。因此，hTLR 2是微生物产物、细胞凋亡和宿主防御机制之间的分子联系。
Apoptosis is implicated in the generation and resolution of inflammation in response to bacterial pathogens. All bacterial pathogens produce lipoproteins (BLPs), which trigger the innate immune response. BLPs were found to induce apoptosis in THP-1 monocytic cells through human Toll-like receptor-2 (hTLR2). BLPs also initiated apoptosis in an epithelial cell line transfected with hTLR2. In addition, BLPs stimulated nuclear factor-kappa B, a transcriptional activator of multiple host defense genes, and activated the respiratory burst through hTLR2. Thus, hTLR2 is a molecular link between microbial products, apoptosis, and host defense mechanisms.