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FcγRIIB作为低亲和力IgG受体介导对多种免疫细胞功能的负反馈调节。它的两种主要分子异构体IIB1、IIB2分布于不同的细胞表面并发挥不同的抑制效应。FcγRIIB可以通过依赖和不依赖于其胞浆区ITIM结构域的方式抑制细胞的激活效应。FcγRIIB在与BCR交联后,抑制BCR与脂筏形成稳定结构,并阻止B细胞的免疫突触形成。FcγRIIB的表达失衡将导致自身免疫病、肿瘤和感染性疾病的发生发展。进一步研究阐明影响FcγRIIB受体表达或其信号传导机制的因素,将有助于人们找到治疗和控制这些疾病的新方法。
FcγRIIB mediates negative feedback regulation of a variety of immune cell functions as a low-affinity IgG receptor. Its two main molecular isoforms IIB1, IIB2 distribute on different cell surfaces and exert different inhibitory effects. FcyRIIB can inhibit the activation of cells through its dependence on and independent of the cytoplasmic ITIM domain. FcyRIIB inhibits the formation of a stable structure between BCR and lipid rafts and prevents the formation of immunological synapses of B cells after crosslinking with BCR. Unbalanced expression of FcγRIIB will lead to the development of autoimmune diseases, tumors and infectious diseases. Further research to elucidate the factors that affect the expression of FcγRIIB receptors or their signaling mechanisms will help to find new ways to treat and control these diseases.