| First Author | Wållberg M | Year | 2011 |
| Journal | J Immunol | Volume | 186 |
| Issue | 4 | Pages | 2543-51 |
| PubMed ID | 21217013 | Mgi Jnum | J:169173 |
| Mgi Id | MGI:4939974 | Doi | 10.4049/jimmunol.1002098 |
| Citation | Wallberg M, et al. (2011) An islet-specific pulse of TGF-(beta) abrogates CTL function and promotes (beta) cell survival independent of Foxp3+ T cells. J Immunol 186(4):2543-51 |
| abstractText | 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 intrapancreatic 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. |
