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甲状腺自主性的免疫病理学发现及甲状腺自身抗体

Immunopathological findings and thyroid autoantibodies in thyroid autonomy.

作者信息

Bretzel R G, Platzer A, Schaeffer R

机构信息

Third Medical Department, Justus-Liebig University, Giessen, FRG.

出版信息

Acta Med Austriaca. 1990;17 Suppl 1:20-4.

PMID:2202177
Abstract

Different phenomena under consideration, lymphocytic and macrophagic infiltration and increased thyrocyte class I and class II antigen expression, normally ascribed to autoimmune thyroid disease (Graves' disease; Hashimoto's thyroiditis) were frequently found in thyroid glands with autonomous nodules, too. Contrary, nodular formations in the vast majority of nodular goiters were not associated with these immunopathological findings. Furthermore, thyroid microsomal, anti-peroxidase and TSH-receptor antibodies although at low frequency rates, were only detected in cases of autonomous nodules but not in cases of nodular goiters. From these findings we conclude that the immune phenomenon observed in thyroid autonomy could not be a consequence of nodular formations but that at least in some cases of thyroid autonomy immunopathogenic mechanisms may play an important role. Based on the fact that class I hyper-expression was more common and that a stronger correlation of cell infiltration with increased class I than with increased class II expression on thyrocytes existed we propose, that if the initial event of the autoimmune process is indeed increased class II expression, this stimulus may more likely originate from increased non-thyrocyte class II positivity (for example dendritic or endothelial cells) than from thyrocyte class II positivity. But, if aberrant class II expression is not the initial stimulus, another candidate could be the increased thyrocyte class I expression observed, probably due to the action of interferon alpha and/or beta induced by any unknown stimulus (viruses?).

摘要

在对不同现象的研究中发现,淋巴细胞和巨噬细胞浸润以及甲状腺细胞I类和II类抗原表达增加(这些通常归因于自身免疫性甲状腺疾病,如格雷夫斯病和桥本甲状腺炎)在伴有自主性结节的甲状腺中也很常见。相反,绝大多数结节性甲状腺肿中的结节形成与这些免疫病理学发现无关。此外,甲状腺微粒体抗体、抗过氧化物酶抗体和促甲状腺激素受体抗体,虽然出现频率较低,但仅在自主性结节病例中检测到,而在结节性甲状腺肿病例中未检测到。从这些发现中我们得出结论,甲状腺自主性中观察到的免疫现象并非结节形成的结果,而是至少在某些甲状腺自主性病例中,免疫致病机制可能发挥重要作用。基于I类高表达更为常见以及细胞浸润与甲状腺细胞I类表达增加的相关性强于与II类表达增加的相关性这一事实,我们提出,如果自身免疫过程的初始事件确实是II类表达增加,那么这种刺激更可能源于非甲状腺细胞II类阳性增加(例如树突状细胞或内皮细胞),而非甲状腺细胞II类阳性。但是,如果异常的II类表达不是初始刺激因素,那么另一个候选因素可能是观察到的甲状腺细胞I类表达增加,这可能是由于任何未知刺激(病毒?)诱导的α干扰素和/或β干扰素的作用。

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