不同浓度碘对体外培养的人甲状腺细胞HLA-DR、CD_(40)、B7.1及Fas表达的影响

Effect of different iodine concentrations on the expressions of HLA-DR,CD_(40),B7.1, and Fas in normal human thyrocytes in vitro

目的 通过研究碘对正常人甲状腺细胞表面免疫相关抗原表达的影响 ,以期在靶细胞水平探讨碘在自身免疫性甲状腺疾病 (AITD)发生发展中的作用机制。方法 传代培养的正常人甲状腺细胞 ,单独以碘化钾刺激或与细胞因子干扰素 (IFN)γ、IFN α共同作用后 ,分析甲状腺细胞表面HLA DR抗原、粘附分子CD4 0 和B7.1分子 (CD80 )及Fas抗原的表达变化。结果 IFN γ能诱导正常人甲状腺细胞表达HLA DR ,碘不影响IFN γ的诱导作用 ;正常人甲状腺细胞表达CD4 0 分子 ,IFN γ能明显促进其表达 ,碘能够协同IFN γ的刺激作用 (P <0 .0 5 ) ;IFN α能刺激甲状腺细胞B7.1的表达 ;碘有增加IFN α诱导的甲状腺细胞B7.1表达的趋势 ;正常人甲状腺细胞表达Fas抗原 ,IFN γ能增强其表达 ,碘不影响甲状腺细胞表面Fas的表达。结论 碘可能通过细胞因子等的作用刺激甲状腺细胞CD4 0 和B7.1的表达 。

Objective Toinvestigatetheeffectofiodineon the expressions of HLA DR, CD 40 , B7.1(CD 80 ) and Fas in cultured normal human thyrocytes and to elucidate the role of iodine on the pathogenesis of autoimmune thyroid diseases (AITD). Methods Passaged normal human thyrocytes from normal persons died of accidents were cultured in medium with potassium iodide at graded concentration (1×10 -3 , 1×10 -2 , 5×10 -2 , 2×10 -1 , 1 mmol/L) at the presence or absence of interferon (IFN) γ (0.1 U/L), IFN α (1 μg/L) for 72 hours. HLA DR, CD 40 , B7.1 and Fas antigen expressions of cultured thyrocytes induced by these stimulators were examined using immunofluorescence staining analyzed by flow cytometer. Results Normal human thyrocytes did not express HLA DR. IFN γ could significantly stimulate HLA DR expression in cultured thyrocytes (P<0.05). Iodide did not influence IFN γ stimulated HLA DR expression of thyrocytes. Cultured normal human thyrocytes expressed CD 40 and obviously increased CD 40 expression by the stimulation of IFN γ. Iodide did not stimulate CD 40 expression alone, but upregulated CD 40 expression in these cells stimulated by IFN γ (P<0.05). IFN α enhanced B7.1 expression, iodide did not affect B7.1 expression alone, but tended to upregulate B7.1 expression induced by IFN α in these cells. Fas antigen was originally expressed on the surface of thyrocytes and upregulated by IFN γ, but iodide did not regulate the expression of Fas in these cells. Conclusion IodidestimulatestheexpressionsofCD 40 and B7.1 in cultured thyroidcytes by the effect of cytokines and participates in the pathogeneses of AITD.