NDLI: The clinical and immunological signi fi cance of GAD-speci fi c autoantibody and T-cell responses in type 1 diabetes

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The clinical and immunological signi fi cance of GAD-speci fi c autoantibody and T-cell responses in type 1 diabetes

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Author	Boettler, Tobias Pagni, Philippe P. Jaffe, Rachel Cheng, Yang Zerhouni, Peter Herrath, Matthias G. Von
Abstract	Antigen-specific interventions are desirable approaches in Type 1 Diabetes (T1D) as they can alter isletspecific autoimmunity without systemic side effects. Glutamic acid decarboxylase of 65 kDa (GAD65) is a major autoantigen in type 1 diabetes (T1D) and GAD-specific autoimmunity is a common feature of T1D in humans but also in mouse models of the disease. In humans, administration of the GAD65 protein in an alum formulation has been shown to reduce C-peptide decline in recently diagnosed patients, however, these observations were not confirmed in subsequent phase II/III clinical trials. As GAD-based immune interventions in different formulations have successfully been employed to prevent the establishment of T1D in mouse models of T1D, we sought to analyze the efficacy of GAD-alum treatment and the effects on the GAD-specific immune response in two different mouse models of T1D. Consistent with the latest clinical trials, mice treated with GAD-alum were not protected from diabetes, although GAD-alum induced a GAD-specific Th2-deviated immune response in transgenic rat insulin promoterglycoprotein (RIP-GP) mice. These observations underline the importance of a thorough, preclinical evaluation of potential drugs before the initiation of clinical trials. 2013 The Authors. Published by Elsevier Ltd. Open access under CC BY license.
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Alternate Webpage(s)	https://mfprac.com/web2018/07literature/literature/Endocrinology/DM1-GAD_Boettler.pdf
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article

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