Role of adapters in Toll-like receptor signalling

被引:40
作者
Akira, S
Yamamoto, M
Takeda, K
机构
[1] Osaka Univ, Microbial Dis Res Inst, Dept Host Def, Suita, Osaka 5650871, Japan
[2] Japan Sci & Technol Corp, ERATO, Suita, Osaka 5650871, Japan
关键词
immune response; interleukin; interferon; Myd88; signal transduction; Toll-like receptor(TLR);
D O I
10.1042/bst0310637
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Toll-like receptors (TLRs) play a critical role in the detection of invading pathogens within the body and the subsequent immune response. individual TLRs recognize distinct microbial components. The TLRs are a type 1 transmembrane receptor that possess an extracellular leucine-rich repeat domain and cytoplasmic domain homologous with that of the interleukin 1 receptor (IL-1R) family. Upon stimulation, TLR recruits the IL-1R-associated kinase (IRAK) via the adapter MyD88, ultimately leading to the activation of nuclear factor-kappaB. Cytokine production in response to all TLR ligands is completely abolished in MyD88-deficient cells, indicating that MyD88 is an essential signalling molecule shared among members of the IL-1R/Toll family. However, several novel adaptor molecules have recently been identified. Evidence is now accumulating showing that differential utilization of these adaptors may activate overlapping as well as distinct signalling pathways, and ultimately give rise to distinct biological effects exerted by individual TIER family members.
引用
收藏
页码:637 / 642
页数:6
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