正常人和自身免疫性甲状腺疾病患者甲状腺细胞对碘致抗原表达的不同敏感性

Different sensitivity of thyroid cells of normal and AITD patients to iodide on inducing antigen expression

目的探讨碘对体外培养的G raves病(GD)、桥本甲状腺炎(HT)、正常人甲状腺滤泡上皮细胞(TEC)抗原表达的影响。方法分离培养正常、GD和HT TEC,给予不同浓度NaI干预,免疫组化检测各组TEC CD54、HLA-DR表达的水平,流式细胞仪检测各组细胞CD80水平的变化,同时放免测定培养液中细胞因子TNF-α、IL-1β水平;观察加碘前后抗原表达的变化。结果NaI可以使GD、HT患者TEC表达的CD54和HLA-DR增加HT的CD80表达增加(P<0.05),并使培养液中细胞因子TNF-α、IL-1β分泌增加(P<0.05);但NaI不能使正常TEC表达上述抗原(P>0.05)。结论CD54、CD80和HLA-DR在AITD的免疫学发病机制中起重要作用;碘可以作为一个重要的环境因子,通过与局部环境中的细胞因子及其它免疫炎症介质的协同作用间接影响作为抗原提呈细胞(antigen present cell,APC)而激活的TEC,碘不是AITD的始发因素,但在AITD的易感个体或者已有早期免疫功能紊乱的隐性患者,碘可能增加甲状腺局部细胞因子如IL-1β等分泌,使相应抗原表达上调,导致AITD的发生。

Objective To explore the effects of iodide on inducing the expressions of CD54, CD80 and HLA-DR on thyroid follicular epithelial cells （TEC） from control, Graves disease （GD） patients and hyperthyroid （TH） patients. Methods After primary TEC of control, GD and HT patients were cultured with different dose of iodide, the expressions of CD54 and HLA-DR on TEC in vitro were determined by immunohistoehemieal methods, the expression of CD80 was detected by flow eytometry. TNF-α and IL-Iβ in culture supernatants were confirmed by radioimmunoassay. Results Iodide could increase the expressions of CD54, HLA-DR on TEC from GD, HT patients and CD80 from HT patients, but had no effect on normal TEC. Conclusion Abnormal expression of CD54, CD80 and HLA-DR may play an important role in the pathogenesis of AITD. Excessive iodide as an important environmental factor acts on TEC activated by eytokine and some increased cell membrane antigen in local thyroid gland, and maintains the autoimmune reaction. Iodide is not the initial factor, but can up-regulate the secretion of IL-1β and the expression of membrane antigen in some AITD susceptible and latent cases so as to induce the incidence of AITD.