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Diabetes 54:107-115, 2005
© 2005 by the American Diabetes Association, Inc.

Autoimmune Diabetes and Resistance to Xenograft Transplantation Tolerance in NOD Mice

Ethel J. Gordon1, Linda S. Wicker2, Laurence B. Peterson3, David V. Serreze4, Thomas G. Markees1, Leonard D. Shultz4, Aldo A. Rossini1, Dale L. Greiner1, and John P. Mordes1

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

Costimulation blockade induces prolonged rat islet and skin xenograft survival in C57BL/6 mice. Nonobese diabetic (NOD) mice, which are used to model human autoimmune diabetes, are resistant to costimulation blockade-induced allograft tolerance. We tested the hypothesis that NOD mice would also be resistant to costimulation blockade-induced rat xenograft tolerance. We report that rat islet xenograft survival is short in spontaneously diabetic NOD mice treated with a tolerizing regimen of donor-specific transfusion and anti-CD154 antibody. Rat islet xenograft survival is only marginally longer in chemically diabetic NOD mice treated with costimulation blockade but is prolonged further in NOD Idd congenic mice bearing C57-derived chromosome 3 loci. Reciprocally, the presence of NOD-derived chromosome 3 loci shortens islet xenograft survival in tolerized C57BL/6 mice. Islet xenograft survival is longer in tolerized NOD.CD4a–/– and (NOD x C57BL/6)F1 mice than in NOD mice but still much shorter than in C57BL/6 mice. Skin xenograft survival in (NOD x C57BL/6)F1 mice treated with costimulation blockade is short, suggesting a strong genetic resistance to skin xenograft tolerance induction. We conclude that the resistance of NOD mice to xenograft tolerance induction involves some mechanisms that also participate in the expression of autoimmunity and other mechanisms that are distinct.

Address correspondence and reprint requests to Dr. Dale L. Greiner, University of Massachusetts Medical School, Diabetes Division, Department of Medicine, 373 Plantation St., Biotech 2, Suite 218, Worcester, MA 01605. E-mail: dale.greiner{at}umassmed.edu


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Copyright © 2005 by the American Diabetes Association.