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Graves病(GD)是一种自身免疫性甲状腺疾病,其发病机制涉及到细胞免疫与体液免疫的异常。新近的研究发现,调节性T细胞(Treg)能够抑制那些逃避的自身反应性T细胞克隆的活性和功能,在自身免疫性甲状腺疾病发病的发生发展中扮演重要角色。在GD的发病过程中,不仅有自身反应性T细胞的参与,也可有抑制免疫反应的自身反应性Treg的参与。而Treg及其表面表达分子叉头/翅膀状螺旋(Foxp3)基因、糖皮质类固醇激素诱导的肿瘤坏死因子受体家族相关受体(GITR)及细胞毒性T淋巴细胞相关抗原(CTLA)-4的高表达可减少GD等自身免疫性疾病的发生。因此提高Treg的反应性,进而抑制自身免疫,是GD很有希望的治疗策略。
Graves disease (GD) is an autoimmune thyroid disease whose pathogenesis involves abnormal cellular and humoral immunity. Recent studies have found that Tregs can inhibit the activity and function of those self-reactive T cell clones that evade and play an important role in the pathogenesis of autoimmune thyroid diseases. In the pathogenesis of GD, not only the involvement of autoreactive T cells, but also the immune response of autoreactive Tregs involved. Treg and its surface expression of the molecular fork / wing helix (Foxp3) gene, glucocorticoid-induced tumor necrosis factor receptor family related receptor (GITR) and cytotoxic T lymphocyte antigen (CTLA) -4 High expression can reduce the occurrence of autoimmune diseases such as GD. Therefore, to improve the reactivity of Treg and then to suppress autoimmunity is a very promising therapeutic strategy for GD.