IL-10 is necessary and sufficient for autoimmune diabetes in conjunction with NOD MHC homozygosity

Myung Shik Lee, Regula Mueller, Linda S. Wicker, Laurence B. Peterson, Nora Sarvetnick

Research output: Contribution to journalArticlepeer-review

106 Scopus citations

Abstract

Contrary to expectations based on in vitro experiments, we previously found that pancreatic IL-10 did not inhibit autoimmune diabetes but accelerated it in an MHC-dependent manner. Therefore, the ability of IL-10 to overcome the absence of all non-MHC diabetes susceptibility (Idd) alleles was studied in transgenic mice expressing pancreatic IL-10 backcrossed to B10.H2(g7) congenic mice, which have no Idd alleles other than NOD MHC (H2(g7)). IL-10 transgenic backcross 1 (BC1) mice with H2(g7/g7) haplotype developed clear-cut insulitis and diabetes, but neither transgenic mice with the H2(g/b) haplotype nor nontransgenic BCL mice did so. Further implicating IL-10 in autoimmune diabetes, anti-IL-10 antibody treatment inhibited the development of insulitis in NOD mice. These results suggest that IL-10 may be necessary and sufficient for producing autoimmune diabetes in conjunction with NOD MHC homozygosity and that some Idd genes may be related to the regulation of IL-10.

Original languageEnglish (US)
Pages (from-to)2663-2668
Number of pages6
JournalJournal of Experimental Medicine
Volume183
Issue number6
DOIs
StatePublished - Jun 1 1996

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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