First Author | Hawiger D | Year | 2008 |
Journal | J Immunol | Volume | 180 |
Issue | 5 | Pages | 3140-7 |
PubMed ID | 18292537 | Mgi Jnum | J:131529 |
Mgi Id | MGI:3773932 | Doi | 10.4049/jimmunol.180.5.3140 |
Citation | Hawiger D, et al. (2008) ICOS mediates the development of insulin-dependent diabetes mellitus in nonobese diabetic mice. J Immunol 180(5):3140-7 |
abstractText | Initiation of diabetes in NOD mice can be mediated by the costimulatory signals received by T cells. The ICOS is found on Ag-experienced T cells where it acts as a potent regulator of T cell responses. To determine the function of ICOS in diabetes, we followed the course of autoimmune disease and examined T cells in ICOS-deficient NOD mice. The presence of ICOS was indispensable for the development of insulitis and hyperglycemia in NOD mice. In T cells, the deletion of ICOS resulted in a decreased production of the Th1 cytokine IFN-gamma, whereas the numbers of regulatory T cells remained unchanged. We conclude that ICOS is critically important for the induction of the autoimmune process that leads to diabetes. |