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An update on the pathogenesis of Hashimoto's thyroiditis

机译:桥本氏甲状腺炎发病机制研究进展

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摘要

It is 70 years since Noel Rose embarked on his pioneering studies that lead to the discovery of autoimmune thyroiditis and the elucidation of Hashimoto's thyroiditis. This short review to honour his passing focuses on the developments in our understanding of the causes and pathogenesis of HT over the last five years. Recent genetic studies have reported heritability estimates for HT and associated diseases for the first time, and emphasised the complexity of the genetic factors involved, including monogenic forms of HT. Environmental factors continue to be elucidated, especially as a side effect of drugs which modulate the immune system therapeutically. Regarding pathogenetic mechanisms, multiple cytokine networks have been identified which involve the thyroid cells in a circuit of escalating proinfiammatory effects, such as the expression of infiammasome components, and an array of different defects in T regulatory cells may underlie the loss of self-tolerance to thyroid autoantigens. Finally, a number of studies have revealed fresh insights into disease associations with HT which may have both pathological and clinical significance, the most intriguing of which is a possible direct role of the autoimmune process itself in causing some of the persistent symptoms reported by a minority of patients with levothyroxine-treated HT.
机译:70年前,诺埃尔·罗斯(Noel Rose)开始了他的开创性研究,这些研究导致了自身免疫性甲状腺炎的发现和桥本氏甲状腺炎的阐明。这篇纪念他逝世的简短评论侧重于我们在过去五年中对 HT 病因和发病机制的理解发展。最近的遗传学研究首次报道了HT和相关疾病的遗传力估计,并强调了所涉及的遗传因素的复杂性,包括HT的单基因形式。 环境因素继续被阐明,特别是作为治疗性调节免疫系统的药物的副作用。关于发病机制,已经确定了多种细胞因子网络,这些网络涉及甲状腺细胞的促生殖作用,例如infiammasome成分的表达,并且T调节细胞中的一系列不同缺陷可能是对甲状腺自身抗原的自我耐受性丧失的基础。最后,许多研究揭示了与HT的疾病关联的新见解,这可能具有病理学和临床意义,其中最有趣的是自身免疫过程本身可能在引起少数左旋甲状腺素治疗HT患者报告的一些持续症状中发挥直接作用。

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