Takeda Kiyoshi, Akira Shizuo
Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, and SORST of Japan Science and Technology Corporation, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan.
Cell Microbiol. 2003 Mar;5(3):143-53. doi: 10.1046/j.1462-5822.2003.00264.x.
Toll receptors in insects, mammals and plants are key players that sense the invasion of pathogens. Toll-like receptors (TLRs) in mammals have been established to detect specific components of bacterial and fungal pathogens. Furthermore, recent evidence indicates that TLRs are involved in the recognition of viral invasion. Signalling pathways via TLRs originate from the conserved Toll/IL-1 receptor (TIR) domain. The TIR domain-containing MyD88 acts as a common adaptor that induces inflammatory cytokines; however, there exists a MyD88-independent pathway that induces type I IFNs in TLR4 and TLR3 signalling. Another TIR domain-containing adaptor, TIRAP/Mal has recently been shown to mediate the MyD88-dependent activation in the TLR4 and TLR2 signalling pathway. Thus, individual TLRs may have their own signalling systems that characterize their specific activities.
昆虫、哺乳动物和植物中的Toll受体是感知病原体入侵的关键参与者。哺乳动物中的Toll样受体(TLR)已被证实可检测细菌和真菌病原体的特定成分。此外,最近的证据表明TLR参与病毒入侵的识别。通过TLR的信号通路源自保守的Toll/IL-1受体(TIR)结构域。含TIR结构域的MyD88作为一种常见的衔接蛋白,可诱导炎性细胞因子;然而,存在一条不依赖MyD88的通路,该通路在TLR4和TLR3信号传导中诱导I型干扰素。另一种含TIR结构域的衔接蛋白TIRAP/Mal最近被证明可介导TLR4和TLR2信号通路中依赖MyD88的激活。因此,单个TLR可能具有其自身的信号系统,这些信号系统表征了它们的特定活性。
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