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格雷夫斯病中的促甲状腺激素受体自身抗体。

Thyrotropin receptor autoantibodies in Graves' disease.

作者信息

Schott Matthias, Scherbaum Werner A, Morgenthaler Nils G

机构信息

Department of Endocrinology, Diabetes and Rheumatology, Heinrich-Heine-University of Düsseldorf, 40225 Düsseldorf, Germany.

出版信息

Trends Endocrinol Metab. 2005 Jul;16(5):243-8. doi: 10.1016/j.tem.2005.05.009.

Abstract

Clinical thyrotoxicosis in Graves' disease patients is caused by thyrotropin receptor (TSHR)-stimulating autoantibodies. The molecular mechanisms of TSHR post-translational modification, TSHR signaling and TSHR-autoantibody interaction are still debatable, and the precise interaction of stimulating and blocking autoantibodies with TSHR is unclear. Recent TSHR epitope studies indicate that binding sites for stimulating and blocking autoantibodies are close together, not on distinct or distant parts of the molecule. Furthermore, new methods to detect TSHR autoantibodies and their clinical use are addressed. Highly sensitive TSHR autoantibody assays are widely available and cost efficient, and their routine clinical use might help in the differential diagnosis of hyperthyroidism and disease outcome prediction in patients with high levels of TSHR autoantibodies.

摘要

格雷夫斯病患者的临床甲状腺毒症是由促甲状腺素受体(TSHR)刺激自身抗体引起的。TSHR翻译后修饰、TSHR信号传导以及TSHR-自身抗体相互作用的分子机制仍存在争议,刺激和阻断自身抗体与TSHR的确切相互作用尚不清楚。最近的TSHR表位研究表明,刺激和阻断自身抗体的结合位点彼此靠近,而非位于分子的不同或遥远部位。此外,还讨论了检测TSHR自身抗体的新方法及其临床应用。高灵敏度TSHR自身抗体检测方法广泛可用且成本效益高,其在临床常规应用可能有助于甲状腺功能亢进的鉴别诊断以及TSHR自身抗体水平高的患者疾病转归的预测。

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