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    Islet allograft survival induced by costimulation blockade in NOD mice is controlled by allelic variants of Idd3

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    Authors
    Pearson, Todd
    Weiser, Peter
    Markees, Thomas G.
    Serreze, David V.
    Wicker, Linda S.
    Peterson, Laurence B.
    Cumisky, Anne-Marie
    Shultz, Leonard D.
    Mordes, John P.
    Rossini, Aldo A.
    Greiner, Dale L.
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    UMass Chan Affiliations
    Department of Medicine, Division of Endocrinology and Metabolism
    Department of Medicine, Diabetes Division
    Program in Immunology and Virology
    Graduate School of Biomedical Sciences
    Document Type
    Journal Article
    Publication Date
    2004-07-28
    Keywords
    Alleles; Animals; CD40 Ligand; Combined Modality Therapy; Diabetes Mellitus, Type 1; Graft Survival; Immunotherapy; Islets of Langerhans Transplantation; Mice; Mice, Inbred C57BL; Mice, Inbred NOD; Transplantation, Homologous; Variation (Genetics)
    Life Sciences
    Medicine and Health Sciences
    
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    Link to Full Text
    https://doi.org/10.2337/diabetes.53.8.1972
    Abstract
    NOD mice develop type 1 autoimmune diabetes and exhibit genetically dominant resistance to transplantation tolerance induction. These two phenotypes are genetically separable. Costimulation blockade fails to prolong skin allograft survival in (NOD x C57BL/6)F1 mice and in NOD-related strains made diabetes-resistant by congenic introduction of protective major histocompatibility complex (MHC) or non-MHC Idd region genes. Here, we tested the hypothesis that the genetic basis for the resistance of NOD mice to skin allograft tolerance also applies to islet allografts. Surprisingly, costimulation blockade induced permanent islet allograft survival in (NOD x C57BL/6)F1 mice but not in NOD mice. After costimulation blockade, islet allograft survival was prolonged in diabetes-resistant NOD.B6 Idd3 mice and shortened in diabetes-free C57BL/6 mice congenic for the NOD Idd3 variant. Islet allograft tolerance could not be induced in diabetes-resistant NOD.B10 Idd5 and NOD.B10 Idd9 mice. The data demonstrate that 1) NOD mice resist islet allograft tolerance induction; 2) unlike skin allografts, resistance to islet allograft tolerance is a genetically recessive trait; 3) an Idd3 region gene(s) is an important determinant of islet allograft tolerance induction; and 4) there may be overlap in the mechanism by which the Idd3 resistance locus improves self-tolerance and the induction of allotolerance.
    Source

    Diabetes. 2004 Aug;53(8):1972-8.

    DOI
    10.2337/diabetes.53.8.1972
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/34327
    PubMed ID
    15277375
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    Link to article in PubMed

    ae974a485f413a2113503eed53cd6c53
    10.2337/diabetes.53.8.1972
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