Development of Insulin-Dependent Diabetes Mellitus Does Not Depend on Specific Expression of the Human Endogenous Retrovirus HERV-K
Development of Insulin-Dependent Diabetes Mellitus Does Not Depend on Specific Expression of the Human Endogenous Retrovirus HERV-K
复制标题
胰岛素依赖性糖尿病的发生并不依赖于人内源性逆转录病毒 HERV-K 的特异性表达
DOI：
10.1016/s0092-8674(00)81776-6
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发表时间：
1998
期刊：
影响因子：
64.5
通讯作者：
H. Wagner
中科院分区：
文献类型：
--
作者：
R. Löwer;R. Tönjes;K. Boller;J. Denner;Bernd Kaiser;R. Phelps;J. Löwer;R. Kurth;K. Badenhoop;H. Donner;K. Usadel;T. Miethke;M. Lapatschek;H. Wagner
胰岛素依赖型糖尿病（Insulin-dependent diabetes mellitus，IDDM）是一种β细胞特异性、T细胞介导的自身免疫性疾病。去年，Bernard Conrad及其同事提出，β细胞破坏是由于内源性逆转录病毒（HERV-K）编码的超抗原在抗原呈递细胞表面表达导致自身反应性T细胞的系统性活化所致（Conrad et al. 1997）。通过观察两名患者的T细胞受体链Vβ7家族的胰腺富集，开始了对这种假定超抗原的研究。在这里，我们提出的研究结果与这一有趣的假设相矛盾。
Insulin-dependent diabetes mellitus (IDDM) is a β cell–specific, T cell–mediated autoimmune disease. Last year, Bernard Conrad and coworkers proposed that the β cell destruction is caused by the systemic activation of autoreactive T cells due to the expression of a superantigen encoded by an endogenous retrovirus (HERV-K) on the surface of antigen-presenting cells (Conrad et al. 1997). The search for this putative superantigen had been initiated by the observation of a pancreatic enrichment of the Vβ7 family of T cell receptor chains in two patients. Here we present findings contradicting this intriguing hypothesis.