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首页> 外文期刊>Cytokine >Interferon-alpha, -beta and -gamma induce CXCL9 and CXCL10 secretion by human thyrocytes: modulation by peroxisome proliferator-activated receptor-gamma agonists.
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Interferon-alpha, -beta and -gamma induce CXCL9 and CXCL10 secretion by human thyrocytes: modulation by peroxisome proliferator-activated receptor-gamma agonists.

机译：干扰素-α，-β和-γ诱导人甲状腺细胞分泌CXCL9和CXCL10：由过氧化物酶体增殖物激活的受体-γ激动剂调节。

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摘要

It has been hypothesized that interferon (IFN) alpha and beta cause autoimmune thyroid dysfunctions by changing the Th1/Th2 balance, but the mechanisms involved are not yet known. The aims of this study were: (a) to test the effect of IFNalpha, IFNbeta and IFNgamma on the secretion of the Th1 chemokines CXCL9 and CXCL10, in "primary cultures of human thyroid follicular cells" (TFC); (b) to assess the effect of PPARgamma activation on CXCL9 and CXCL10 secretion. In TFC, CXCL9 and CXCL10 were undetectable in the supernatant. IFNgamma, IFNalpha and IFNbeta, dose dependently induced CXCL9 and CXCL10 release. TNFalpha alone had no effect. The combination of each of the IFNs with TNFalpha had a significant synergistic effect on CXCL9 and CXCL10 secretion. Treatment of TFC with rosiglitazone dose dependently inhibited the IFNs-stimulated CXCL9 and CXCL10 release. Compared with IFNalpha and IFNbeta, IFNgamma was the most potent stimulus of CXCL9 and CXCL10 secretion. In conclusion, IFNalpha, IFNbeta, IFNgamma and TNFalpha (synergistically with IFNs) dose-dependently induce the release of CXCL9 and CXCL10 by TFC, suggesting that this process may be related, at least in part, to the appearance of thyroid dysfunction during IFNs therapy. Furthermore, PPARgamma activation partially inhibits this process.
机译：据推测，干扰素（IFN）α和β可通过改变Th1 / Th2平衡而引起自身免疫性甲状腺功能低下，但所涉及的机制尚不清楚。这项研究的目的是：（a）在“人甲状腺滤泡细胞原代培养”（TFC）中测试IFNalpha，IFNbeta和IFNgamma对Th1趋化因子CXCL9和CXCL10分泌的影响; （b）评估PPARgamma活化对CXCL9和CXCL10分泌的影响。在TFC中，上清液中未检测到CXCL9和CXCL10。 IFNgamma，IFNalpha和IFNbeta剂量依赖性地诱导CXCL9和CXCL10释放。单独使用TNFalpha无效。每种IFN与TNFα的组合对CXCL9和CXCL10的分泌具有明显的协同作用。用罗格列酮治疗TFC剂量依赖性地抑制了IFNs刺激的CXCL9和CXCL10释放。与IFNalpha和IFNbeta相比，IFNgamma是CXCL9和CXCL10分泌的最有力刺激。总之，IFNα，IFNβ，IFNγ和TNFalpha（与IFN协同作用）剂量依赖性地诱导TFC释放CXCL9和CXCL10，这表明该过程至少部分与IFN治疗期间甲状腺功能障碍的出现有关。 。此外，PPARgamma激活会部分抑制该过程。

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