自体角朊细胞通过B7-H1介导对异种混合淋巴细胞增殖的抑制作用  

Autologuos keratinocytes suppress xenogeneic mixed lymphocyte reaction by inducible expression of B7-H1 molecule

作　　者：周芸[1] 焦志军[1] 辛利军[1] 汪四七 路丽明[1] 丁庆[1] 周晓荣[1] 杨能[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 [2]上海博康生殖医院,上海200030

出　　处：《现代免疫学》2009年第6期486-490,共5页Current Immunology

基　　金：国家自然科学基金重点项目(30530690);国家自然科学基金面上项目(30772018);上海市科委项目(07JC14033)

摘　　要：为了探讨自体角朊细胞诱导免疫抑制的机制,我们利用已建立的MELR体外增殖系统,采用三色标记流式细胞术及定量PCR方法检测了自体角朊细胞共信号分子B7-H1和HLA II类分子的表达情况,观察其对角朊细胞所诱导的免疫抑制的影响。结果发现,自体而非异体角朊细胞可有效抑制MELR。在抑制系统中检测到B7-H1和II类分子高表达于自体角朊细胞表面。单抗封阻B7-H1,可逆转自体角朊细胞诱导的免疫抑制作用。结论:自体角朊细胞通过B7-H1介导对异种混合淋巴细胞增殖的抑制作用。To explore the mechanism underlying the keratinocyte-induced suppression, mixed swine endothelial-lymphocyte cul ture （MELC） system was established, and the expression of co signal molecule B7 HI and HLA class II molecules on autol oguos keratinocytes was examined by using three-colour flow cytometry and real-time PCR. It was found that the strong suppression of xenogeneic lymphoproliferation was induced by autologous, instead of allogeneic, keratinocytes when superimposed on MEI,C as moducing cells. The autologuos keratinocytes expressed high level of B7-H1 and HLA II molecules after addition to MELC or simply stimulated with IFN-γ. Anti-B7-H1 mAbs could block the keratinocyte-induced suppression. It is concluded that the suppression of MELR by autologuos keratinocytes can be mediated by the co-signal molecule B7 -H1.

关 键 词：免疫抑制 B7-H1 异种混合淋巴细胞增殖反应 

分 类 号：R392.4[医药卫生—免疫学]