The Journal of Immunology
• Type I diabetes (T1D), which results from autoimmune destruction of insulin-producing β-cells, is known to be orchestrated by Th1 CD4 cells.
• Unlike the established contribution of Th1 CD4 cells, the contribution of Th17 CD4 cells to T1D, which secrete IL-17, is controversial.
• We show that Th17 cells can be reprogrammed to Th1 cells in response to pancreatic inflammation.
• Prevention of Th1 cell development by deficiencies of Stat4, IFN-γR, and IFN-γ resulted in diabetes elicited by Th17 cells.
• This study identifies a new mechanism by which Th17 cells contribute to diabetes.