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• W2046971036 endingPage "1499" @default.
• W2046971036 startingPage "1494" @default.
• W2046971036 abstract "The 65-kDa isoform of glutamic acid decarboxylase (GAD65) has been implicated in autoimmune diabetes in NOD mice, but the role of the 67-kDa GAD isoform (GAD67) is less clear. We found that immunization of 4-week-old NOD mice with purified recombinant mouse GAD67 prevented or significantly delayed the onset of diabetes. To further explore this phenomenon, we characterized anti-GAD67 immune responses in naive and GAD-immunized NOD mice. Anti-GAD67 antibodies titers were relatively low in naive mice at all ages, but a single immunization with GAD67 at 4 weeks induced high titers of anti-GAD antibodies by 6 weeks of age. In both 4-week-old and diabetic NOD mice, there were significant endogenous T-cell proliferative responses against purified recombinant mouse GAD67. These T-cell proliferative responses were blocked by anti-I-ANOD and anti-CD4 antibodies. To characterize the anti-GAD T-cell responses in the NOD mice, we established T-cell lines and T-cell clones which recognized GAD67, and we used recombinant subfragments of GAD to localize the predominant T-cell epitopes in GAD67. T-cells from naive NOD mice proliferated in response to all GAD subfragments, whereas T-cells from diabetic mice responded primarily to the COOH-terminal 83 amino acids of GAD67. These results suggest that GAD67 is an autoantigen in IDDM and immunization of prediabetic NOD mice with GAD67 can prevent the onset of diabetes." @default.
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• W2046971036 date "1994-12-01" @default.
• W2046971036 modified "2023-10-11" @default.
• W2046971036 title "Immunization With the Larger Isoform of Mouse Glutamic Acid Decarboxylase (GAD67) Prevents Autoimmune Diabetes in NOD Mice" @default.
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• W2046971036 doi "https://doi.org/10.2337/diab.43.12.1494" @default.
• W2046971036 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/7525393" @default.
• W2046971036 hasPublicationYear "1994" @default.
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