| First Author | Jhala G | Year | 2022 |
| Journal | Cell Rep | Volume | 39 |
| Issue | 4 | Pages | 110747 |
| PubMed ID | 35476975 | Mgi Jnum | J:325263 |
| Mgi Id | MGI:7283961 | Doi | 10.1016/j.celrep.2022.110747 |
| Citation | Jhala G, et al. (2022) Interferons limit autoantigen-specific CD8(+) T-cell expansion in the non-obese diabetic mouse. Cell Rep 39(4):110747 |
| abstractText | Interferon gamma (IFNgamma) is a proinflammatory cytokine implicated in autoimmune diseases. However, deficiency or neutralization of IFNgamma is ineffective in reducing disease. We characterize islet antigen-specific T cells in non-obese diabetic (NOD) mice lacking all three IFN receptor genes. Diabetes is minimally affected, but at 125 days of age, antigen-specific CD8(+) T cells, quantified using major histocompatibility complex class I tetramers, are present in 10-fold greater numbers in Ifngr-mutant NOD mice. T cells from Ifngr-mutant mice have increased proliferative responses to interleukin-2 (IL-2). They also have reduced phosphorylated STAT1 and its target gene, suppressor of cytokine signaling 1 (SOCS-1). IFNgamma controls the expansion of antigen-specific CD8(+) T cells by mechanisms which include increased SOCS-1 expression that regulates IL-2 signaling. The expanded CD8(+) T cells are likely to contribute to normal diabetes progression despite reduced inflammation in Ifngr-mutant mice. |
