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自身免疫性糖尿病(AID)是一种病因和发病机制尚未完全阐明的,由T细胞介导的胰岛β细胞选择性破坏的自身免疫性疾病。最近研究发现瘦素可与胰岛β细胞、免疫细胞及细胞因子相互作用、相互影响,可能在AID自身免疫损伤中的多个环节上发挥重要作用,因其具体机制非常复杂,并存在不少不明之处。叉头蛋白是FOX蛋白家族成员之一,主要表于CD+CD25+T细胞,参与体内免疫系统的调节,尤其可影响CD+CD25+调节性T细胞的发育和功能。AID患者体内CD+CD25+T细胞减少,诱导叉头蛋白3的表达或过度转CD+CD25+T细胞,有可能预防AID。
Autoimmune diabetes mellitus (AID) is an autoimmune disease that is selectively destroyed by T cell-mediated islet beta cells, an etiology and pathogenesis of which is not fully elucidated. Recent studies have shown that leptin interacts with and interacts with islet beta cells, immune cells and cytokines and may play an important role in various aspects of AID autoimmune injury because of the complexity of the mechanism and the unknown Where. Forkhead protein, a member of the FOX protein family, is predominantly expressed on CD + CD25 + T cells and is involved in the regulation of the immune system in vivo and in particular on the development and function of CD + CD25 + regulatory T cells. It is possible to prevent AID by reducing CD + CD25 + T cells in AID patients, inducing expression of prion protein 3 or over-converting CD + CD25 + T cells.