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IL-1 Receptor Deficiency Slows Progression to Diabetes in the NOD Mouse

¹ St. Vincent’s Institute of Medical Research, Fitzroy, Australia
² Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia
³ Department of Microbiology and Infectious Diseases and Julia McFarlane Diabetes Research Centre, Faculty of Medicine, University of Calgary, Alberta, Canada
⁴ Department of Microbiology and Immunology, University of Melbourne, Parkville, Victoria, Australia

Proinflammatory cytokines are believed to be important in pancreatic ß-cell destruction in the development of type 1 diabetes. They act by upregulation of genes including Fas and inducible nitric oxide synthase (iNOS), which have both been shown to lead to ß-cell death in vitro. We used mice deficient in the interleukin (IL)-1 receptor (IL-1R) to assess the contribution of IL-1 to different models of diabetes. IL-1R-deficient islets were protected from the damaging effects of tumor necrosis factor (TNF) and interferon (IFN)- in vitro, and ß-cell expression of iNOS was reduced, suggesting that IL-1 mediates the induction of iNOS by TNF and IFN-. IL-1 action was not required for induction of class I major histocompatibility complex or Fas by TNF and IFN-. IL-1R-deficient nonobese diabetic (NOD) mice developed diabetes significantly slower than wild-type mice. IL-1R deficiency did not affect diabetes in 8.3 TCR transgenic NOD mice but prolonged the time to diabetes in BDC2.5 TCR transgenic NOD mice. We conclude that IL-1R deficiency slows progression to diabetes in NOD mice but on its own does not prevent diabetes.

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