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Diabetes 52:321-326, 2003
© 2003 by the American Diabetes Association, Inc.

NOD Congenic Mice Genetically Protected From Autoimmune Diabetes Remain Resistant to Transplantation Tolerance Induction

Todd Pearson1, Thomas G. Markees2, Linda S. Wicker3, David V. Serreze1,2,4, Laurence B. Peterson5, John P. Mordes2, Aldo A. Rossini1,2,6, and Dale L. Greiner1,2

1 Program in Immunology and Virology, the University of Massachusetts Medical School, Worcester, Massachusetts
2 Department of Medicine, the University of Massachusetts Medical School, Worcester, Massachusetts
3 Juvenile Diabetes Research Foundation/Wellcome Trust Diabetes and Inflammation Laboratory, University of Cambridge, Cambridge, U.K
4 The Jackson Laboratory, Bar Harbor, Maine
5 Department of Pharmacology, Merck Research Laboratories, Rahway, New Jersey
6 Department of Molecular Medicine, the University of Massachusetts Medical School, Worcester, Massachusetts

The loss of self-tolerance leading to autoimmune type 1 diabetes in the NOD mouse model involves at least 19 genetic loci. In addition to their genetic defects in self-tolerance, NOD mice resist peripheral transplantation tolerance induced by costimulation blockade using donor-specific transfusion and anti-CD154 antibody. Hypothesizing that these two abnormalities might be related, we investigated whether they could be uncoupled through a genetic approach. Diabetes-resistant NOD and C57BL/6 stocks congenic for various reciprocally introduced Idd loci were assessed for their ability to be tolerized. Surprisingly, in NOD congenic mice that are almost completely protected from diabetes, costimulation blockade failed to prolong skin allograft survival. In reciprocal C57BL/6 congenic mice with NOD-derived Idd loci, skin allograft survival was readily prolonged by costimulation blockade. These data indicate that single or multiple combinations of evaluated Idd loci that dramatically reduce diabetes frequency do not correct resistance to peripheral transplantation tolerance induced by costimulation blockade. We suggest that mechanisms controlling autoimmunity and transplantation tolerance in NOD mice are not completely overlapping and are potentially distinct, or that the genetic threshold for normalizing the transplantation tolerance defect is higher than that for preventing autoimmune diabetes.


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