國家衛生研究院 NHRI:Item 3990099045/14053
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    题名: Alpha-lipoic acid inhibits spontaneous diabetes and autoimmune recurrence in non-obese diabetic mice by enhancing differentiation of regulatory T cells and showed potential for use in cell therapies for the treatment of type 1 diabetes
    作者: Huang, SH;Kuo, SL;Chen, SJ;Lin, JR;Chen, YW;Hong, ZJ;Sytwu, HK;Lin, GJ
    贡献者: National Institute of Infectious Diseases and Vaccinology
    摘要: Type 1 diabetes (T1D) is caused by the destruction of β cells in pancreatic islets by autoimmune T cells. Islet transplantation has been established as an effective treatment for T1D. However, the survival of islet grafts is often disrupted by recurrent autoimmunity. Alpha-lipoic acid (ALA) has been reported to have immunomodulatory effects and, therefore, may have therapeutic potential in the treatment of T1D. In this study, we investigated the therapeutic potential of ALA in autoimmunity inhibition. We treated non-obese diabetic (NOD) mice with spontaneous diabetes and islet-transplantation mice with ALA. The onset of diabetes was decreased and survival of the islet grafts was extended. The populations of Th1 cells decreased, and regulatory T cells (Tregs) increased in ALA-treated mice. The in vitro Treg differentiation was significantly increased by treatment with ALA. The adoptive transfer of ALA-differentiated Tregs into NOD recipients improved the outcome of the islet grafts. Our results showed that in vivo ALA treatment suppressed spontaneous diabetes and autoimmune recurrence in NOD mice by inhibiting the Th1 immune response and inducing the differentiation of Tregs. Our study also demonstrated the therapeutic potential of ALA in Treg-based cell therapies and islet transplantation used in the treatment of T1D.
    日期: 2022-01-21
    關聯: International Journal of Molecular Sciences. 2022 Jan 21;23(3):Article number 1169.
    Link to: http://dx.doi.org/10.3390/ijms23031169
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1422-0067&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000932993900001
    Cited Times(Scopus): https://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85123010222
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