巨细胞病毒衣壳蛋白UL11抗原肽介导类风湿关节炎发病的分子机制研究

类风湿关节炎（RA）是一种高致残性自身免疫病，但其发病机制尚不明确，但已有研究发现，人巨细胞病毒（HCMV）感染是RA发生的重要因素之一。近期，本课题组在RA患者的血清中首次发现，HCMV表面的衣壳蛋白UL11的27-31位氨基酸（UL11(27-31)）多肽的抗体为特异性致病抗体，前期研究还发现该抗原可影响T细胞功能。本项目将利用RA样本资源和成熟的RA鼠模型，以UL11(27-31)多肽对T细胞亚群功能的影响为研究主线，从分子机制、细胞功能、动物模型、RA患者四个方面探讨HCMV通过UL11(27-31)多肽对T细胞分化及功能的调控作用、细胞因子产生及RA发病的基本机制，为RA的诊断和治疗提供新的理论基础和研究方向。

Rheumatoid arthritis(RA) is an autoimmune disease with high morbidity, however, little is known about the definite mechanism. Studies have showed the importance of human cytomegalovirus(HCMV) in the pathogenesis of Rheumatoid arthritis. Recently, our studies have demonstrated an antibody against HCMV UL11(27-31)peptide is high expressed in patients with RA and influenced the function of T cells in peripheral blood. In this project, we propose to use T cells from patients with RA and RA mouse model to investigate the effects of HCMV UL11(27-31)peptide on T cell subsets . We aim to explore the potential role of HCMV UL11(27-31)peptide involving in etiology of RA, and further providing new methods for the treatment of RA.