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  • Title: Glutamic acid decarboxylase epitope protects against autoimmune diabetes through activation of Th2 immune response and induction of possible regulatory mechanism.
    Author: Gong Z, Pan L, Le Y, Liu Q, Zhou M, Xing W, Zhuo R, Wang S, Guo J.
    Journal: Vaccine; 2010 May 28; 28(24):4052-8. PubMed ID: 20406664.
    Abstract:
    Oral tolerance mediated by autoantigens has been applied successfully as a potential therapeutic strategy for preventing and treating autoimmune diseases. We previously showed cholera toxin B subunit (CTB) is an efficient mucosal carrier molecule for induction of systemic T cell tolerance to linked insulin antigens. In this study, we used an oral antigen consisting of a fusion protein composed of CTB and triple copies of glutamic acid decarboxylase 65 (GAD65) peptides 531-545 (3p531) to test its in vivo effect and investigate the mechanism of immune tolerance. Non-obese diabetic mice fed microgram quantities of the CTB-3p531 fusion protein showed a prominent reduction in pancreatic islet inflammation and a delay in the development of diabetes. Increased anti-GAD65 IgG1, serum IgA and unchanged IgG2a antibodies titers; together with an increase of IL-4, IL-10 production and a decrease of IFN-gamma production suggested possible activation of GAD65-specific Th2 immune responses. Adoptive transfer of splenocytes indicated oral administration of CTB-3p531 fusion protein generated potent regulatory cells that can suppress diabetogenic T cells. This study demonstrates the CTB-3p531 fusion protein protects against autoimmune diabetes by generation of regulatory T cells and induction of immunological tolerance.
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