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Updated: Jul 30, 2026

Accelerated Type 1 Diabetes Induction in Mice by Adoptive Transfer of Diabetogenic CD4+ T Cells
Published on: May 6, 2013
IL-10 deficiency does not inhibit insulitis and accelerates cyclophosphamide-induced diabetes in the nonobese
B Balasa1, K Van Gunst, N Jung
1Department of Immunology, The Scripps Research Institute, La Jolla, California 92037, USA.
Abstract:
IL-10 exterts profound immunostimulatory and immunoinhibitory effects. To explore the role of IL-10 in autoimmune diabetes of nonobese diabetic (NOD) mice, we generated IL-10-deficient NOD mice. In contrast to our previous results with neutralizing antibodies to IL-10, IL-10-deficient NOD mice developed insulitis and their splenocytes readily responded to islet antigen glutamic acid decarboxylase 65. IL-10-deficient NOD mice did not develop accelerated spontaneous diabetes. On the other hand, IL-10-deficient NOD mice developed accelerated disease following cyclophosphamide (CYP) injection. These findings demonstrate that IL-10 is dispensable for autoimmune diabetes. IL-10's absence fails to accelerate endogenous diabetes but potentiates CYP-induced diabetes.
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