One amino acid difference is critical for suppression of the development of experimental autoimmune diabetes (EAD) with intravenous injection of insulinB:9-23 peptide

  • Okumachi Y
  • Moriyama H
  • Kameno M
 et al. 
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Abstract

InsulinB:9-23 peptide (insB:9-23) reactive T cells has been reported as crucial for type 1 diabetes. In this study, experimental autoimmune diabetes (EAD) mice, which subcutaneous immunization of ins1 or 2B:9-23 induced autoimmune diabetes in F1(B7.1B6 × BALB/c), was investigated for antigen specific therapy to delete pathogenic T cells. Intravenous injection of ins1 or 2B:9-23 significantly delayed the development of diabetes on the corresponding peptide-induced EAD (ins1EAD or ins2EAD) concomitant with reduced insulitis and insulin autoantibodies expression. Population of Foxp3+CD4+T cell was unchanged whereas the level of anti-insB:9-23 specific IgG2abut not IgG1were specifically decreased, suggesting reduction of pathogenic insB:9-23 reactive T cells. Most interestingly, intravenous administration of ins2B:9-23, whose amino acid sequence had one amino acid difference at position 9 delayed the development of diabetes in both ins1EAD and ins2EAD whereas ins1B:9-23 administration delayed diabetes in the ins1EAD but not ins2EAD, suggesting that one amino acid difference gives critical influence on the effect of intravenous injection of antigenic peptide for type 1 diabetes. © 2008 Elsevier Inc. All rights reserved.

Author-supplied keywords

  • Antigen specific therapy
  • Insulin
  • Type 1 diabetes

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Authors

  • Yasuyo Okumachi

  • Hiroaki Moriyama

  • Mami Kameno

  • Takashi Arai

  • Minoru Kishi

  • Midori Kurohara

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