The novel antigen-specific immune regulation for pathogenic CD8+ T cells

开发一种以抗原特异性方式下调免疫反应而不引起全身免疫抑制的治疗手段是可取的。我们尝试通过表达抗原和免疫抑制分子（如TRAIL或PD-L1）的小鼠ES细胞来源的树突状细胞（ES- dcs）对致病性CD8+ T细胞的免疫调节。在此期间，我们引入了c蛋白诱导的肌炎（CIM），这是一种由致病性CD8+ T细胞引起的疾病模型。制备了表达免疫抑制分子的功能分子- dcs。这些es - dc可能预防致病性cd8 + T细胞衍生的自身免疫性疾病。

It is desirable to develop a therapeutic means to down-modulate immune responses in anantigen-specific manner without causing systemic immune suppression. We tried the immune regulationof pathogenic CD8+ T cells by mouse ES cell-derived dendritic cells (ES-DCs) expressing both antigenand immunosuppressive molecule, such as TRAIL or PD-L1. In this period, we brought in the C-proteininduced myositis, CIM, which was disease model caused by pathogenic CD8+ T cells. The functionalES-DCs expressing immunosuppressive molecule was prepared. These ES-DCs may prevent pathogenicCD8+ T cells-derived autoimmune disease.