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Differential protection in two transgenic lines of NOD/Lt mice hyperexpressing the autoantigen GAD65 in pancreatic beta-cells.

  1. M Bridgett,
  2. M Cetkovic-Cvrlje,
  3. R O'Rourke,
  4. Y Shi,
  5. S Narayanswami,
  6. J Lambert,
  7. V Ramiya,
  8. S Baekkeskov and
  9. E H Leiter
  1. The Jackson Laboratory, Bar Harbor, Maine 04609, USA.
    Diabetes 1998 Dec; 47(12): 1848-1856. https://doi.org/10.2337/diabetes.47.12.1848
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    Abstract

    Although expressed at very low levels in islets of NOD mice, GAD65 is a candidate islet autoantigen. Two transgenic lines of NOD/Lt mice expressing high levels of human GAD65 from a rat insulin promoter were generated. Transgenes were integrated on proximal chromosome 15 of the A line and on the Y chromosome of the Y line. Transgenic A-line mice were obligate hemizygotes, since homozygous expression resulted in developmental lethality. A twofold higher level of hGAD65 transcripts in A-line islets from young donors was associated with higher GAD protein and enzyme activity levels. Y-line males developed diabetes at a similar rate and incidence as standard NOD/Lt males. In contrast, A-line mice of both sexes exhibited a markedly lowered incidence of diabetes. Insulitis, present in both transgenic lines, developed more slowly in A-line mice and correlated with a reduction in the ratio of gamma-interferon to interleukin-10 transcripts. Splenic leukocytes from young A-line donors transferred diabetes into NOD-scid recipients at a retarded rate compared with those from nontransgenic donors. Further, nontransgenic NOD T-cells transferred diabetes more slowly in NOD-scid recipients that were congenic for A-line transgenes as compared with standard NOD-scid recipients. Primed T-cell responses and spontaneous humoral reactivity to GAD65 failed to distinguish transgenic from nontransgenic mice. Quantitative differences in expression level or insertional mutagenesis are possible mechanisms of protection in the A line.

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    December 1998, 47(12)
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    Differential protection in two transgenic lines of NOD/Lt mice hyperexpressing the autoantigen GAD65 in pancreatic beta-cells.
    M Bridgett, M Cetkovic-Cvrlje, R O'Rourke, Y Shi, S Narayanswami, J Lambert, V Ramiya, S Baekkeskov, E H Leiter
    Diabetes Dec 1998, 47 (12) 1848-1856; DOI: 10.2337/diabetes.47.12.1848

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    Differential protection in two transgenic lines of NOD/Lt mice hyperexpressing the autoantigen GAD65 in pancreatic beta-cells.
    M Bridgett, M Cetkovic-Cvrlje, R O'Rourke, Y Shi, S Narayanswami, J Lambert, V Ramiya, S Baekkeskov, E H Leiter
    Diabetes Dec 1998, 47 (12) 1848-1856; DOI: 10.2337/diabetes.47.12.1848
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