论文部分内容阅读
1型糖尿病是一种由T细胞介导的胰腺β细胞进行性损伤的自身免疫性疾病,当β细胞大量被破坏时,胰岛素分泌不足引起血糖升高甚至酮症酸中毒症状。该病的发病机制与自身抗原有关,包括胰岛素、谷氨酸脱羧酶(GAD)、酪氨酸酶样蛋白(IA2),这些抗原的暴露可引起体内一系列的自身免疫过程。通常认为,自身反应T细胞(auto reactive CD4+effector T cells,Teffs)通过分泌IFN-γ和
Type 1 diabetes is an autoimmune disease that is progressive damage of pancreatic beta cells mediated by T cells. Insufficient insulin secretion leads to hyperglycemia and even symptoms of ketoacidosis when large numbers of beta cells are destroyed. The pathogenesis of this disease is related to autoantigens, including insulin, glutamate decarboxylase (GAD), tyrosinase-like protein (IA2), and the exposure of these antigens can cause a series of autoimmune processes in the body. It is generally accepted that auto reactive CD4 + effector T cells (Teffs)