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1型糖尿病与肠道病毒感染密切相关。多数病毒通过诱发自身免疫而致病,其机制有分子相似性和旁路激活学说。前者证实,病毒的非结构蛋白2C有6个氨基酸序列与谷氨酸脱羧酶抗原相同,故能诱发自身免疫破坏;后者认为,感染导致胰腺外分泌组织炎症,激活休眠的T细胞而诱发免疫反应。研究证实,病毒诱发自身免疫反应要在一定数量的自主反应性T细胞及胰岛感染存在的前提下才会发生,在糖尿病出现临床症状几年前,β-细胞破坏就已经开始。
Type 1 diabetes and enterovirus infection are closely related. Most viruses cause disease by inducing autoimmunity, and their mechanisms are molecular similarities and bypass activation theories. The former confirmed that the virus non-structural protein 2C has 6 amino acid sequence and glutamate decarboxylase antigen the same, it can induce autoimmune damage; the latter that the infection leads to pancreatic exocrine inflammation, activation of dormant T cells and induce immune response . Studies have shown that virus-induced autoimmune reactions occur only in the presence of a number of autoreactive T cells and pancreatic islets, and beta-cell disruption has already begun a few years prior to the onset of clinical symptoms of diabetes.