An Islet-Specific Pulse of TGF-beta Abrogates CTL Function and Promotes beta Cell Survival Independent of Foxp3(+) T Cells

作者：Wallberg Maja; Wong F Susan; Green E Allison^*

来源：The Journal of Immunology, 2011, 186(4): 2543-2551.

DOI：10.4049/jimmunol.1002098

Effective therapies that prevent chronic inflammation from developing into type 1 diabetes remain elusive. In this study, we show that expression of TGF-beta for just 1 wk in inflamed islets of NOD mice significantly delays diabetes development. Time course studies demonstrated that the brief TGF-beta pulse protects only if administered when extensive beta cell destruction has occurred. Surprisingly, TGF-beta-mediated protection is not linked to enhanced Foxp3(+) regulatory T cell activity or to decreased intra-pancreatic presentation of islet Ags. Instead, TGF-beta disables the transition of primed autoreactive CD8(+) T cells to cytotoxic effectors and decreases generation, or maintenance, of CD8(+) memory T cells within the pancreas, significantly impairing their diabetogenic capacity. The Journal of Immunology, 2011, 186: 2543-2551.

• 出版日期2011-2-15
• 单位河北医科大学