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消除胰岛自身免疫。

Deleting islet autoimmunity.

作者信息

Liu Edwin, Li Marcella, Jasinski Jean, Kobayashi Masakazu, Gianani Roberto, Nakayama Maki, Eisenbarth George S

机构信息

Barbara Davis Center for Childhood Diabetes, Department of Pediatrics, University of Colorado Health Sciences Center, Aurora, CO, USA.

出版信息

Cell Biochem Biophys. 2007;48(2-3):177-82. doi: 10.1007/s12013-007-0022-9.

Abstract

Even though there are numerous autoantigens for type 1 diabetes, current evidence suggests that a single autoantigen, namely insulin, is responsible for the key initiating event in autoimmunity. If a single autoantigen is necessary for triggering the autoimmune process, then antigen-specific therapy to block or delete the immune response against that autoantigen before epitope spreading occurs, may become a larger focus of future immunotherapeutic strategies. In this article, we review current literature regarding insulin as an autoantigen and potential approaches to deleting insulin-reactive T cells through the use of peptide vaccines and targeted T cell receptor immunizations.

摘要

尽管1型糖尿病存在众多自身抗原,但目前的证据表明,单一自身抗原,即胰岛素,是自身免疫关键起始事件的罪魁祸首。如果单一自身抗原是触发自身免疫过程所必需的,那么在表位扩展发生之前,通过抗原特异性疗法来阻断或消除针对该自身抗原的免疫反应,可能会成为未来免疫治疗策略的更大焦点。在本文中,我们综述了有关胰岛素作为自身抗原的当前文献,以及通过使用肽疫苗和靶向T细胞受体免疫来清除胰岛素反应性T细胞的潜在方法。

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