期刊
JOURNAL OF IMMUNOLOGY
卷 180, 期 5, 页码 3140-3147出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.180.5.3140
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- Howard Hughes Medical Institute Funding Source: Medline
- NIDDK NIH HHS [P30-DK-45735] Funding Source: Medline
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.
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