Low frequency of autoantibodies to the human Na+/I- symporter in patients with autoimmune thyroid disease

Low frequency of autoantibodies to the human Na+/I- symporter in patients with autoimmune thyroid disease
复制标题

DOI:
10.1210/jc.85.12.4630
复制
发表时间:
2000-12-01
影响因子:
5.8
通讯作者:
Morgenthaler, MG
Morgenthaler, MG
中科院分区:
医学2区
文献类型:
--
作者:
Seissler, J;Wagner, S;Morgenthaler, MG

文献摘要

被引文献

相似文献

多项研究表明,碘化钠同向转运蛋白(NIS)可能是甲状腺自身免疫性疾病中的主要自身抗原。本文的目的是探讨人 NIS 自身抗体 (hNIS-Ab) 在桥本甲状腺炎 (HT) 和格雷夫斯病 (GD) 患者中的重要性。从甲状腺组织中克隆全长人 NIS (hNIS),在 [S-35] 蛋氨酸存在下通过体外转录和翻译表达,并用于在直接结合测定中分析自身抗体。结构相似的葡萄糖转运蛋白 GLUT-2 与对照蛋白在同一系统中产生。放射自显影显示全长 hNIS 被表达,被 NIS 单克隆抗体识别,并与自身免疫性甲状腺疾病患者的一些血清强烈结合,该血清不与 GLUT-2 对照蛋白发生反应。使用健康对照的第 95.2 个百分位作为阳性阈值,177 名 GD 患者中的 19 名 (10.7%) 和 72 名 HT 患者中的 15 名 (20.8%) 分别具有 hNIS-Ab。采用更严格的截止标准(正常对照的 99.4%),仅 5.6% 的 GD 患者和 6.9% 的 HT 患者中发现 hNIS-Ab。与 GD 和正常对照相比,HT 中观察到 hNIS-Ab 水平显着升高 (P < 0.001)。 hNIS-Ab 与 TSH 受体抗体无相关性,仅与甲状腺过氧化物酶抗体相关性较弱(P < 0.05)。个体血清中 hNIS-Ab、甲状腺过氧化物酶和 TSH 受体抗体的比较表明,额外检测 hNIS-Ab 并不会增加 GD 或 HT 的诊断能力。我们的数据表明,hNIS 并不是自身免疫性甲状腺疾病的主要抗原,因为它是仅少数 GD 和 HT 患者体液自身免疫的靶标。 hNIS-Ab 的出现频率可能低于之前研究报道的频率。
Several studies suggest that the sodium-iodide symporter (NIS) may represent a major autoantigen in autoimmune diseases of the thyroid. The aim of the present paper was to investigate the importance of autoantibodies to human NIS (hNIS-Ab) in patients suffering from Hashimoto's thyroiditis (HT) and Graves' disease (GD). Full-length human NIS (hNIS) was cloned from thyroid tissue, expressed by in vitro transcription and translation in the presence of [S-35]methionine, and used to analyze autoantibodies in a direct binding assay. The structurally similar glucose transporter, GLUT-2, was produced in the same system as control protein. Autoradiography revealed that full-length hNIS was expressed, recognized by a NIS monoclonal antibody, and strongly bound by some sera from patients with autoimmune thyroid disease, which did not react with the GLUT-2 control protein. Using the 95.2th percentile of healthy controls as threshold for positivity, 19 of 177 (10.7%) patients with GD and 15 of 72 (20.8%) patients with HT had hNIS-Ab, respectively. Applying more stringent cut-off criteria (99.4th percentile of normal controls), hNIS-Ab were found in only 5.6% of patients with GD and 6.9% of patients with HT. In HT significantly higher hNIS-Ab levels were observed compared with GD and normal controls (P < 0.001). There was no correlation between hNIS-Ab and TSH receptor antibodies and only a weak correlation to thyroid peroxidase antibodies (P < 0.05). Comparison of hNIS-Ab, thyroid peroxidase, and TSH receptor antibodies in individual sera revealed that the additional detection of hNIS-Ab did not increase the diagnostic power for GD or HT. Our data indicate that hNIS is not a major antigen in autoimmune thyroid disease, as it is the target of humoral autoimmunity in only a few patients with GD and HT. The frequency of hNIS-Ab may be lower than that reported in previous studies.