辅助性T细胞免疫与桥本甲状腺炎

Helper T cell immune and Hashimoto＇s thyroiditis

桥本甲状腺炎（HT）是一种自身免疫性疾病,其免疫发病机制与T细胞亚群中的CD4＋ CD25＋调节性T细胞、辅助性T细胞（Th） 17、滤泡辅助性T细胞有重要关系.CD4＋ CD25＋调节性T细胞可抑制Th1介导的自身免疫和炎性反应,其减少势必使Thl过量产生细胞因子（包括白细胞介素-1β、干扰素-γ、肿瘤坏死因子-α）,这些细胞因子激发了甲状腺细胞的凋亡,从而促使HT的发生.Th17与调节性T细胞相拮抗,其在早期HT患者中高表达.滤泡辅助性T细胞是淋巴组织中最重要的效应性T细胞亚群之一,其过量表达会引起HT的发生.对调节性T细胞、Th17、滤泡辅助性T细胞进行研究,有助于进一步认识HT的免疫发病机制.

Hashimoto＇s thyroiditis （HT） is an autoimmune disease,the immune pathogenesis of which has important relationship with T cell subgroup of CD4 ＋ CD25 ＋ regulatory T cells,helper T cells（Th）17 and T follicular helper cells.Inflammation and autoimmunity triggered by Th1 can be suppressd by regulatory T cells.Its reduction will inevitably make excessive production of Th1 cytokines,including interleukin1β,interferon-γ,tumor necrosis factor-α.These cytokines promote thyroid cell apoptosis,which result in the occurrence of HT.T follicular helper cells in lymphoid tissue is one of the most important T cell subsets,their overexpression can cause HT.Th17 is antagonism of regulatory T cells,and overexpressed in patients with early HT.Study of the regulatory T cells and Th17,T follicular helper cells will help us to further understand the immune pathogenesis of HT.