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首页> 外文期刊>Endocrinology >Influence of signal transducer and activator of transcription-1 signaling on thyroid morphology and function.
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Influence of signal transducer and activator of transcription-1 signaling on thyroid morphology and function.

机译：信号转导和转录激活因子-1对甲状腺形态和功能的影响。

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摘要

Interferon (IFN)-gamma has been involved in the pathogenesis of Hashimoto thyroiditis. It is a cytokine released by infiltrating mononuclear cells that mediates its actions mainly through signal transducer and activator of transcription-1 (STAT1) but also through other transcription factors. To dissect the effect of IFN gamma on thyroid morphology and function, we crossed transgenic mice that express IFN gamma specifically in the thyroid gland to mice deficient in STAT1. Lack of STAT1 ameliorated the abnormal thyroid morphology and the primary hypothyroidism typical of IFN gamma transgenic mice but not the suppressed iodine accumulation. Interestingly, lack of STAT1 alone decreased iodine accumulation, seemingly through expression of TGFbeta. These results indicate that STAT1 is required to mediate some but not all of the phenotypic changes induced by IFN gamma and that it also regulates iodine accumulation via TGFbeta signaling.
机译：干扰素（IFN）-γ已参与桥本甲状腺炎的发病机理。它是通过渗透单核细胞释放的细胞因子，主要通过信号转导和转录激活因子-1（STAT1）以及其他转录因子介导其作用。为了剖析IFNγ对甲状腺形态和功能的影响，我们将在甲状腺中特异性表达IFNγ的转基因小鼠与STAT1缺陷小鼠杂交。 STAT1的缺乏改善了IFNγ转基因小鼠的异常甲状腺形态和典型的原发性甲状腺功能减退症，但并未抑制碘的积累。有趣的是，单独的STAT1缺乏似乎通过TGFbeta的表达降低了碘的积累。这些结果表明，STAT1是介导某些但不是全部由IFNγ诱导的表型变化所必需的，并且它还通过TGFbeta信号传导调节碘的积累。

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