Regulation of autoimmune diabetes by non-islet-specific T cells - A role for the glucocorticoid-induced TNF receptor

Anish Suri, Jun Shimizu, Jonathan D. Katz, Shimon Sakaguchi, Emil R. Unanue, Osami Kanagawa

Research output: Contribution to journalArticle

24 Scopus citations

Abstract

Diabetogenic BDC2.5 CD4 T cells induce diabetes when injected into NOD.scid mice. However, when co-transferred with the OVA-specific DO11. 10 CD4 T cells, BDC2.5 T cells failed to cause diabetes. This inhibition depended upon the stimulation of DO11. 10 T cells only with soluble OVA, which skewed their differentiation to a Th2-type pattern of cytokine secretion in vivo. However, in vivo neutralization of IL-4, IL-10 or TGF-β using monoclonal antibodies did not prevent the inhibition whereas treatment with an antibody against the glucocorticoid-incluced TNF receptor abrogated the protection from disease. In the protected mice, the diabetogenic T cells could be isolated from their spleens and shown to transfer diabetes when injected into new NOD.scid recipients. Thus, the inhibition took place without the physical or functional elimination of the diabetogenic T cells.

Original languageEnglish
Pages (from-to)447-454
Number of pages8
JournalEuropean Journal of Immunology
Volume34
Issue number2
DOIs
StatePublished - Feb 1 2004

Keywords

  • Autoimmunity
  • Bystander suppression
  • Diabetes
  • GITR
  • Regulation

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