Abstract
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-γ, 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.
Original language | English (US) |
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Pages (from-to) | 3140-3147 |
Number of pages | 8 |
Journal | Journal of Immunology |
Volume | 180 |
Issue number | 5 |
DOIs | |
State | Published - Mar 1 2008 |
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology