TLR2型
TLR4型
受体
先天免疫系统
Toll样受体
模式识别受体
细胞生物学
肽聚糖
病原相关分子模式
脂多糖
信号转导
生物
脂质A
免疫系统
跨膜蛋白
微生物学
免疫学
细菌
生物化学
遗传学
作者
Shizuo Akira,Katsuaki Hoshino,Tsuneyasu Kaisho
出处
期刊:Journal of Endotoxin Research
[SAGE]
日期:2000-10-01
卷期号:6 (5): 383-387
被引量:77
标识
DOI:10.1177/09680519000060050901
摘要
Toll-like receptors (TLRs) are phylogenetically conserved receptors that recognize pathogen associated molecular patterns (PAMPS). We previously generated mice lacking TLR2 and TLR4 and showed the differential role of TLR2 and TLR4 in microbial recognition. TLR4 functions as the transmembrane component of the lipopolysaccharide (LPS) receptor, while TLR2 recognizes peptidoglycan from Gram-positive bacteria and lipoprotein. We also generated mice lacking MyD88, an adaptor involved in IL-1R/TLR signalings. The responses to a variety of bacterial components were completely abrogated in MyD88-deficient cells. However, unlike the signaling mediated by other bacterial components such as lipoprotein and bacterial DNA, activation of NF-kappaB and MAP kinases was induced in response to LPS even in the absence of MyD88, which indicates the existence of a MyD88-independent pathway. We have recently found that the MyD88-independent pathway is involved in LPS-induced maturation of dendritic cells (DCs).
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