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    Immunology. 2008 Apr;123(4):547-54. Epub 2007 Nov 14.

    Modulation of diabetes in NOD mice by GAD65-specific monoclonal antibodies is epitope specific and accompanied by anti-idiotypic antibodies.

    Hall TR, Bogdani M, Leboeuf RC, Kirk EA, Maziarz M, Banga JP, Oak S, Pennington CA, Hampe CS.

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    Department of Medicine, University of Washington, Seattle, WA 98195, USA.

    Abstract

    Type 1 diabetes is caused by the autoimmune destruction of pancreatic beta cells. Here we show that administration of a human monoclonal antibody (b96.11) specific to the 65-kDa isoform of glutamate decarboxylase (GAD65) to prediabetic non-obese diabetic (NOD) mice significantly delays the onset of autoimmune diabetes. We found this effect to be epitope-specific, as only b96.11 showed this therapeutic property, while a GAD65-specific human monoclonal control antibody (b78) derived from the same patient, but specific to a different determinant of GAD65, had no significant effect on the progression of disease. Administration of b96.11 or b78 to NOD mice was accompanied by the generation of anti-idiotypic antibodies. Importantly, the induced anti-idiotypic antibodies were specific for the immunizing antibody and blocked the binding of GAD65 by the respective antibody. These findings suggest a potential role for the internal image of the GAD65 determinant recognized by b96.11 in the anti-idiotypic antibody, supporting an immunomodulatory role for GAD65-specific autoantibodies, as originally postulated by Jerne.

    PMID:
    18005036
    [PubMed - indexed for MEDLINE]
    PMCID:
    PMC2433323
    Free PMC Article

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