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Interferons limit autoantigen-specific CD8+ T-cell expansion in the non-obese diabetic mouse. 2022
Gaurang Jhala, and
Balasubramanian Krishnamurthy, and
Thomas C Brodnicki, and
Tingting Ge, and
Satoru Akazawa, and
Claudia Selck, and
Prerak M Trivedi, and
Evan G Pappas, and
Leanne Mackin, and
Nicola Principe, and
Erwan Brémaud, and
David J De George, and
Louis Boon, and
Ian Smyth, and
Jonathan Chee, and
Thomas W H Kay, and
Helen E Thomas
Immunology and Diabetes Unit, St Vincent's Institute, Fitzroy, VIC 3065, Australia.
Interferon gamma (IFNγ) is a proinflammatory cytokine implicated in autoimmune diseases. However, deficiency or neutralization of IFNγ 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). IFNγ 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.
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