小鼠B7H1-Ig融合蛋白诱导免疫抑制的机制研究  

Study on the mechanism underlying the immunosuppression induced by B7H1-Ig fusion protein

作　　者：丁庆[1] 路丽明[1] 周芸[1] 辛利军[1] 江阳[1] 焦志军[1] 周晓荣[1] 周光炎[1] 

机构地区：[1]上海交通大学医学院上海市免疫学研究所,上海200025

出　　处：《现代免疫学》2006年第2期93-97,共5页Current Immunology

基　　金：863项目子课题(2003AA205009);国家自然科学基金资助项目(30170864);上海市科委基金项目(03JC14085)

摘　　要：为了探讨小鼠B7H1-Ig融合蛋白诱导免疫抑制的机制,应用抗CD3抗体协同B7H1-Ig融合蛋白刺激纯化的CD4+T细胞,检测其增殖效应和培养上清细胞因子水平的变化,并观察B7H1-Ig对不同品系小鼠混合淋巴细胞反应的抑制作用。发现B7H1-Ig有引起T细胞先增殖后抑制的现象,其抑制作用通过IL-10、TGF-β和受体PD-1,并有调节性T细胞的参与。研究为B7H1-Ig进一步应用于临床疾病的免疫调控打下基础。To explore the roles of B7H1-Ig fusion protein as an immunosuppressive drug, mouse CD4^＋ T lymphoeytes were stimulated with anti-CD3 mAb plus BYH1-Ig or unrelated mlgG2a antibody. In some cultures, neutralizing mAb to IL-10, TGF-β, PD-1 or IFN-γ were added, respectively, Lymphoproliferatinn was determined by incorporation of ^3H-TdR. The expression of PD-I was measured by flow cytometry and apoptosis was determined by Annexin V staining. The data demonstrates that B7HI-Ig was potent to induce immunosuppression through IL-10, TGF-β and expressing PD-1, which suggesting that Tr1 （type I regulatory T cells） may play an important role. These results implicate that the fusion protein migbt be valuable to develop a new strategy for application to clinical diseases by immune regulation.

关 键 词：B7H1-Ig融合蛋白 免疫抑制 共刺激 调节性T细胞 

分 类 号：R392.11[医药卫生—免疫学]