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Toll样受体(Toll-like receptor,TLR)是人体天然免疫系统的主要参与者,TLR在免疫细胞中广泛表达,通过识别病原体相关分子模式(pathogen-associated molecule pattern,PAMP)来触发免疫应答,而对于TLR信号的调节机制的研究仍然是免疫学及其相关学科的热点领域。CMRF35样分子(CMRF-35-like molecules,CLMs)作为免疫细胞表面受体分子可能参与TLR信号的调节,其中CLM-1和CLM-8通过自身含有的免疫受体酪氨酸抑制基序触发对TLR信号的负向调控作用,而CLM-4通过与带有免疫受体酪氨酸活化基序的接头分子结合,促进TLR信号转导,调节免疫细胞对病原体的应答。对CLMs的深入研究将丰富人们对TLR信号调节分子机制的认识。
Toll-like receptor (TLR) is a major player in the natural immune system. TLR is widely expressed in immune cells and triggers an immune response by identifying the pathogen-associated molecule pattern (PAMP) However, the research on the regulatory mechanism of TLR signaling is still a hot area in immunology and related disciplines. CMRF-35-like molecules (CLMs) as immune cell surface receptor molecules may be involved in the regulation of TLR signaling, CLM-1 and CLM-8 through its own immune receptor tyrosine inhibition motif trigger TLR signaling, whereas CLM-4 promotes TLR signaling by modulating the response of immune cells to pathogens by binding to linker molecules with immunoreceptor tyrosine-activated motifs. In-depth study of CLMs will enrich people’s understanding of the molecular mechanism of TLR signaling.