{"title":"Innate Adaptations","authors":"","doi":"10.1126/scisignal.1942003tw304","DOIUrl":null,"url":null,"abstract":"Viruses, bacteria, and fungi express broadly distinct molecular patterns that activate innate arms of the immune system. Most prominently, the Toll-like receptors (TLRs) use these pathogen-specific cues to elicit intracellular signals that can be either dependent or independent of the Toll/interleukin 1 receptor (TIR) domain-containing adaptor proteins, MyD88 and TIRAP. Yamamoto et al. define a third TIR adaptor, TRIF, as critical for MyD88-independent signaling by particular TLRs. Cells deficient in TRIF failed to initiate either the interferon regulatory factor-3 or nuclear factor κB pathways in response to TLR3 or TLR4 activation, but responded normally to activation of other TLR family members. M. Yamamoto, S. Sato, H. Hemmi, K. Hoshino, T. Kaisho, H. Sanjo, O. Takeuchi, M. Sugiyama, M. Okabe, K. Takeda, S. Akira, Role of adaptor TRIF in the MyD88-independent Toll-like receptor signaling pathway. Science 301, 640-643 (2003). [Abstract] [Full Text]","PeriodicalId":21619,"journal":{"name":"Science's STKE","volume":"14 1","pages":"TW304 - tw304"},"PeriodicalIF":0.0000,"publicationDate":"2003-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Science's STKE","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1126/scisignal.1942003tw304","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Viruses, bacteria, and fungi express broadly distinct molecular patterns that activate innate arms of the immune system. Most prominently, the Toll-like receptors (TLRs) use these pathogen-specific cues to elicit intracellular signals that can be either dependent or independent of the Toll/interleukin 1 receptor (TIR) domain-containing adaptor proteins, MyD88 and TIRAP. Yamamoto et al. define a third TIR adaptor, TRIF, as critical for MyD88-independent signaling by particular TLRs. Cells deficient in TRIF failed to initiate either the interferon regulatory factor-3 or nuclear factor κB pathways in response to TLR3 or TLR4 activation, but responded normally to activation of other TLR family members. M. Yamamoto, S. Sato, H. Hemmi, K. Hoshino, T. Kaisho, H. Sanjo, O. Takeuchi, M. Sugiyama, M. Okabe, K. Takeda, S. Akira, Role of adaptor TRIF in the MyD88-independent Toll-like receptor signaling pathway. Science 301, 640-643 (2003). [Abstract] [Full Text]
病毒、细菌和真菌表现出广泛不同的分子模式,激活免疫系统的先天臂。最突出的是,Toll样受体(TLRs)使用这些病原体特异性线索来诱导细胞内信号,这些信号可以依赖或独立于含有Toll/白细胞介素1受体(TIR)结构域的衔接蛋白MyD88和TIRAP。Yamamoto等人定义了第三种TIR适配器TRIF,对于特定tlr的myd88独立信号至关重要。TRIF缺失的细胞在TLR3或TLR4激活时无法启动干扰素调节因子-3或核因子κB通路,但对其他TLR家族成员的激活反应正常。M. Yamamoto, S. Sato, H. Hemmi, K. Hoshino, T. Kaisho, H. Sanjo, O. Takeuchi, M. Sugiyama, M. Okabe, K. Takeda, S. Akira,受体TRIF在myd88非依赖性toll样受体信号通路中的作用《科学》,2003年第1期。【摘要】【全文】