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CD4 0与其相应配体CD4 0L的相互作用在机体的B细胞免疫、T细胞免疫、肿瘤免疫以及移植免疫中发挥极其重要的作用 ,但其作用机制至今尚未阐明。CD4 0mAb和CD4 0L可分别使CD4 0膜分子产生交联和配基化 ,进而使CD4 0分子多聚化 ,CD4 0分子多聚化是CD4 0信号转导的结构基础和始动因素。新近发现的肿瘤坏死因子受体相关因子 (tumornecrosisfactorreceptor associatedfactors,TRAFs)家族是一组连接CD4 0胞浆结构域与下游信号转导分子的接头蛋白 (adaptors) ,TRAFs分子可以与CD4 0胞浆段不同的结构域结合 ,分别或共同活化相同或不同的下游分子从而介导CD4 0分子的不同信号通路 ,产生广泛而复杂的生物效应。如核转录因子KappaB(NF κB)、丝裂原激活的蛋白激酶 (mitogen activatedproteinkinases MAPK)家族JNK ,ERK和P38的激活等 ;故TRAFs是介导CD4 0分子信号转导的中心分子
The interaction between CD4 0 and its corresponding ligand CD4 0L plays an extremely important role in the B cell immunity, T cell immunity, tumor immunity and transplantation immunity, but its mechanism of action has not been elucidated so far. CD4 0mAb and CD4 0L, respectively, can make the membrane cross-linking and ligandization of CD4 0 molecules, which in turn make CD4 0 multi-molecule, CD4 0 molecule multimerisation is the structural basis and motivation of CD4 0 signal transduction. The recently discovered family of tumor necrosis factor receptor associated factors (TRAFs) is a group of adapters that link the CD4 0 cytoplasmic domain to downstream signaling molecules that can differ from the CD4 0 cytoplasmic segment Of the domain binding, respectively, or jointly activate the same or different downstream molecules to mediate different molecular pathways of CD4 0 molecules, resulting in a wide range of complex biological effects. Such as nuclear factor KappaB (NF κB), mitogen activated protein kinase (mitogen activated protein kinase) family JNK, ERK and P38 activation; so TRAFs are central molecules that mediate CD4 0 signal transduction