| First Author | Thomas HE | Year | 1998 |
| Journal | J Clin Invest | Volume | 102 |
| Issue | 6 | Pages | 1249-57 |
| PubMed ID | 9739059 | Mgi Jnum | J:74622 |
| Mgi Id | MGI:2158881 | Doi | 10.1172/JCI2899 |
| Citation | Thomas HE, et al. (1998) IFN-gamma action on pancreatic beta cells causes class I MHC upregulation but not diabetes. J Clin Invest 102(6):1249-57 |
| abstractText | We have generated transgenic nonobese diabetic (NOD) mice expressing dominant negative mutant IFN-gamma receptors on pancreatic beta cells to investigate whether the direct effects of IFN-gamma on beta cells contribute to autoimmune diabetes. We have also quantitated by flow cytometry the rise in class I MHC on beta cells of NOD mice with increasing age and degree of islet inflammatory infiltrate. Class I MHC expression increases gradually with age in wild-type NOD mice; however, no such increase is observed in the transgenic beta cells. The transgenic mice develop diabetes at a similar rate to that of wild-type animals. This study dissociates class I MHC upregulation from progression to diabetes, shows that the rise in class I MHC is due to local IFN-gamma action, and eliminates beta cells as the targets of IFN-gamma in autoimmune diabetes. |
