IL-10 deficiency does not inhibit insulitis and accelerates cyclophosphamide-induced diabetes in the nonobese diabetic mouse

Balaji Balasa, Kurt Van Gunst, Nadja Jung, Jonathan D. Katz, Nora Sarvetnick

Research output: Contribution to journalArticle

27 Scopus citations


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 anti-bodies 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. (C) 2000 Academic Press.

Original languageEnglish (US)
Pages (from-to)97-102
Number of pages6
JournalCellular Immunology
Issue number2
Publication statusPublished - Jun 15 2000



  • Diabetes
  • IL-10
  • Insulitis
  • NOD

ASJC Scopus subject areas

  • Immunology

Cite this