摘要
自身免疫性疾病是指机体对自身抗原发生免疫应答进而导致自体组织损害的一类疾病,其确切的病因和致病机制至今未阐明。近年来研究发现,共刺激分子肿瘤坏死因子受体超家族成员4(tumor necrosis factor receptor superfamily member 4,TNFRSF4,又称OX40)以及肿瘤坏死因子配体超家族成员4(tumor necrosis factor ligand superfamily member 4,TNFSF4,又称OX40L)对T细胞的增殖以及功能发挥有重要意义,可作为T细胞介导疾病的治疗靶点,是领域研究的热点。文章介绍了OX40/OX40L和T细胞亚群滤泡辅助性T细胞(T follicular helper cell, Tfh)的生物学特性,以及OX40/OX40L信号对Tfh分化和生物学功能的促进作用,进一步讨论OX40/OX40L信号通过作用于Tfh促进自身免疫性疾病发生发展的机制,以及该分子作为潜在治疗靶点的应用价值。
Autoimmune diseases are series of diseases in which abnormal immune response against autoantigen leads to tissue damage. The etiology and pathogenesis of most autoimmune diseases remain elusive. Many recent reports showed that the costimulatory molecule tumor necrosis factor receptor superfamily member 4(TNFRSF4, also known as OX40)and its ligand tumor necrosis factor ligand superfamily member 4(TNFSF4, also known as OX40L)are critical for T cell proliferation and function. Therefore, OX40/OX40L may be the therapeutic target in T cell-mediated diseases and have attracted widespread research interest. This review summarizes the biological characteristics of OX40/OX40L and T follicular helper cell(Tfh), as well as the regulation of OX40 expression on the Tfh surface and the effect of OX40/OX40L signal on the differentiation and biological function of Tfh. The mechanism of Tfh in promoting the development of autoimmune diseases through OX40/OX40L signaling and their value as a potential therapeutic target is also discussed.
作者
王璐
马欣
王勤
WANG Lu;MA Xin;WANG Qin(School of Biology&Basic Medical Sciences,Suzhou Medical College of Soochow University,Suzhou 215123,China)
出处
《现代免疫学》
CAS
北大核心
2023年第2期155-161,共7页
Current Immunology
基金
苏州大学“大学生创新创业训练计划”(201910285055Z)
江苏省高等学校自然科学研究重大项目(20KJA180002)。
