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Acquired pMHC I Complexes Greatly Enhance CD4^+ Th Cell's Stimulatory Effect on CD8^+ T Cell-Mediated Diabetes in Transgenic RIP-mOVA Mice

查看全文 作　　者：Khawaja Ashfaque [1,2]Ahmed;Yufeng [1,2]Xie;Xueshu [1]Zhang;Jim [1]Xiang 高影响力作者 机构地区：[1]Research Unit, Saskatchewan Cancer Agency, Departments of Oncology,Microbiology and Immunology, College of Medicine, University ofSaskatchewan, 20 Campus Drive, Saskatoon, Saskatchewan S7N 4H4,Canada;[2]Ahmed and Xie made the same contribution to the study高影响力机构 出　　处：《Cellular & Molecular Immunology》索引2008年第5卷第6期,共9页高影响力期刊 基　　金：supported by research funds from Canadian Institute of Health Research (MOP 79415, 81228 and 89713) 摘　　要：CD4+ helper T (Th) cells play pivotal roles in induction of CD8+ CTL immunity. However, the mechanism of CD4+ T cell help delivery to CD8+ T cells in vivo is still elusive. In this study, we used ovalbumin (OVA)-pulsed dendritic cells (DCOVA) to activate OT-II mouse CD4+ T cells, and then studied the help effect of these CD4+ T cells on CD8+ cytotoxic T lymphocyte (CTL) responses. We also examined CTL mediated islet β cell destruction which led to diabetes in wild-type C57BL/6 mice and transgenic rat insulin promoter (RIP)-mOVA mice expressing β cell antigen OVA with self OVA-specific tolerance, respectively. In adoptive transfer experiments, we demonstrated that help, in the form of peptide/major histocompatibility complex (pMHC) I acquired from DCOVA by DCOVA activation, was required for induction of OVA-specific CTL responses in C57BL/6 mice. However, in combination with TCR transgenic OT-I mouse CD8+ T cells, the tolerogenic dosage of CD4+ Th cells with acquired pMHC I, but not CD4+ (Kb-/-) Th cells without acquired pMHC I were able to cause diabetes in 8/10 (80%) RIP-mOVA mice. This study thus expands the current knowledge in T cell-mediated autoimmunity and provides insight into the nature of CD4+ T cell-mediated help in CD8+ CTL induction. 关 键 词：CD4+ TH pMHC 1 树枝状细胞 糖尿病
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