CAJ | 학술논문

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.
교본갑상선염(HT)시일충자신면역성질병,기면역발병궤제여T세포아군중적CD4+ CD25+조절성T세포、보조성T세포(Th) 17、려포보조성T세포유중요관계.CD4+ CD25+조절성T세포가억제Th1개도적자신면역화염성반응,기감소세필사Thl과양산생세포인자(포괄백세포개소-1β、간우소-γ、종류배사인자-α),저사세포인자격발료갑상선세포적조망,종이촉사HT적발생.Th17여조절성T세포상길항,기재조기HT환자중고표체.려포보조성T세포시림파조직중최중요적효응성T세포아군지일,기과량표체회인기HT적발생.대조절성T세포、Th17、려포보조성T세포진행연구,유조우진일보인식HT적면역발병궤제.
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.