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人甲状腺细胞对白细胞介素-6释放的调节。

Regulation of interleukin-6 release by human thyrocytes.

作者信息

Weetman A P, Bright-Thomas R, Freeman M

机构信息

Department of Medicine, University of Cambridge Clinical School, Addenbrooke's Hospital.

出版信息

J Endocrinol. 1990 Nov;127(2):357-61. doi: 10.1677/joe.0.1270357.

Abstract

Autoimmune thyroiditis is characterized by lymphocytic accumulation within the thyroid which may be the result, in part, of immunomodulatory cytokine secretion by thyrocytes. We have tested human thyroid cell cultures (n = 9) for interleukin-6 (IL-6) release using two bioassays. IL-6 was detected in all culture supernatants under basal conditions and was increased by gamma-interferon, tumour necrosis factor and TSH in a dose-dependent manner. The bioactivity was confirmed as IL-6 by immunoblotting experiments and could not be accounted for by contamination of the thyroid cell cultures with fibroblasts, lymphocytes or monocytes. Circulating IL-6 levels were not raised in patients with Graves' hyperthyroidism. Exogenous recombinant IL-6 reduced cyclic AMP production in response to TSH when added to thyroid cell cultures. Since IL-6 plays a major role in B cell differentiation and T cell activation, release of IL-6 by thyrocytes may increase the intrathyroidal autoimmune response in Graves' disease and Hashimoto's thyroditis. Our results also suggest that IL-6 may modulate thyroid cell function.

摘要

自身免疫性甲状腺炎的特征是甲状腺内淋巴细胞聚集,这可能部分是甲状腺细胞分泌免疫调节细胞因子的结果。我们使用两种生物测定法检测了人类甲状腺细胞培养物(n = 9)中白细胞介素-6(IL-6)的释放。在基础条件下,所有培养上清液中均检测到IL-6,并且γ-干扰素、肿瘤坏死因子和促甲状腺激素可使其呈剂量依赖性增加。通过免疫印迹实验证实该生物活性为IL-6,且不能用成纤维细胞、淋巴细胞或单核细胞污染甲状腺细胞培养物来解释。格雷夫斯甲状腺功能亢进症患者的循环IL-6水平未升高。当添加到甲状腺细胞培养物中时,外源性重组IL-6可降低促甲状腺激素诱导的环磷酸腺苷生成。由于IL-6在B细胞分化和T细胞活化中起主要作用,甲状腺细胞释放IL-6可能会增加格雷夫斯病和桥本甲状腺炎患者甲状腺内的自身免疫反应。我们的结果还表明,IL-6可能调节甲状腺细胞功能。

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