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 Citations (Scopus)

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 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
Volume202
Issue number2
DOIs
StatePublished - Jun 15 2000

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Inbred NOD Mouse
Interleukin-10
Cyclophosphamide
Type 1 Diabetes Mellitus
Glutamate Decarboxylase
Antigens
Injections

Keywords

  • Diabetes
  • IL-10
  • Insulitis
  • NOD

ASJC Scopus subject areas

  • Immunology

Cite this

IL-10 deficiency does not inhibit insulitis and accelerates cyclophosphamide-induced diabetes in the nonobese diabetic mouse. / Balasa, Balaji; Van Gunst, Kurt; Jung, Nadja; Katz, Jonathan D.; Sarvetnick, Nora.

In: Cellular Immunology, Vol. 202, No. 2, 15.06.2000, p. 97-102.

Research output: Contribution to journalArticle

Balasa, Balaji ; Van Gunst, Kurt ; Jung, Nadja ; Katz, Jonathan D. ; Sarvetnick, Nora. / IL-10 deficiency does not inhibit insulitis and accelerates cyclophosphamide-induced diabetes in the nonobese diabetic mouse. In: Cellular Immunology. 2000 ; Vol. 202, No. 2. pp. 97-102.
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