Mechanism underlying counterregulation of autoimmune diabetes by IL-4

Regula Mueller, Linda M. Bradley, Troy Krahl, Nora Sarvetnick

Research output: Contribution to journalArticle

94 Scopus citations

Abstract

Diabetes in nonobese diabetic (NOD) mice is an autoimmune disease characterized by the destruction of the β cells in the pancreas. We have previously reported that transgenic expression of interleukin-4 (IL-4) counterregulates the disease process, completely protecting NOD mice from insulitis and diabetes. Here we demonstrate the presence of autoreactivity but lack of pathogenicity of the IL-4-regulated lymphocytes. The importance of T cell diversity for the protective effect of IL-4 is demonstrated through breeding with transgenic BDC2.5 mice, which have an almost exclusively monoclonal T cell repertoire. Limitation of T cell diversity abrogated the protection by IL-4. We suggest that 'immune deviation' in NOD-IL-4 mice is mediated by the pancreatic tissue itself, which causes activation of distinct, nonpathogenic T cell specificities.

Original languageEnglish (US)
Pages (from-to)411-418
Number of pages8
JournalImmunity
Volume7
Issue number3
DOIs
StatePublished - Sep 1997

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Infectious Diseases

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