Evolution and integration of innate immune recognition systems: the Toll-like receptors

被引：93

作者：

Takeda, K ^{[1
]}

机构：

[1] Kyushu Univ, Med Inst Bioregulat, Dept Mol Genet, Higashi Ku, Fukuoka 8128582, Japan

来源：

JOURNAL OF ENDOTOXIN RESEARCH | 2005年 / 11卷 / 01期

关键词：

Toll-like receptors (TLRs); innate immune recognition; TLR signaling pathways; TRIF; review;

D O I：

10.1179/096805105225006687

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 [生物化学与分子生物学]; 081704 [应用化学];

摘要：

Toll-like receptors (TLRs) recognize specific components of micro-organisms and trigger the activation of innate immunity. TLR-mediated signaling pathways are now rapidly being elucidated. TLR signaling originates from the cytoplasmic Toll/IL-1 receptor (TIR) domain, which is conserved among all TLRs. Furthermore, TIR domain-containing adaptors, such as MyD88, TRIF, TIRAP and TRAM, play essential roles in TLR signaling. MyD88 is essential for inflammatory cytokine production via all TLRs, whereas TRIF is involved in TLR3- and TLR4-mediated MyD88-independent induction of IFN-beta. Thus, innate immunity represents a skilful system that senses microbial invasion and initiates appropriate immune responses.

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页码：51 / 55

页数：5

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