自发性自身免疫性甲状腺炎发病机制的多基因基础概念。

G Wick
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引用次数: 10

摘要

这篇综述提出了一个自发的、器官特异性自身免疫性疾病的发病机制概念,该概念考虑了免疫调节的改变、调节激素的影响和基因决定的目标器官对自身免疫性攻击的主要易感性。肥胖株(OS)鸡的自发性遗传性自身免疫性甲状腺炎模型证明了这一概念。就免疫系统功能的改变而言,MHC相关(Ir)和非MHC相关基因都参与其中。MHC即某一单倍型仅对自发性自身免疫性甲状腺炎的发生频率和严重程度起调节作用,而某些非MHC相关基因的存在是该病发生的绝对先决条件。后者也适用于基因决定的靶器官易感性,而激素因素,尤其是性类固醇和糖皮质激素,同样只具有兼性调节作用。只有存在与非mhc编码的异常免疫功能和编码甲状腺对自身免疫过程易感性的基因相关的适当遗传群时,才会发生严重的自身免疫性甲状腺。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Concept of a multigenic basis for the pathogenesis of spontaneous autoimmune thyroiditis.

The review presents a concept for the pathogenesis of spontaneous, organ-specific autoimmune diseases that take into account an altered immune regulation, modulating hormonal influences and a genetically determined primary susceptibility of the target organ for the autoimmune attack. The concept is exemplified by means of the Obese strain (OS) chicken model which develops a spontaneous hereditary autoimmune thyroiditis. In respect to the the altered function of the immune system both, MHC associated (Ir) and non-MHC associated genes are involved. The MHC, i.e. a certain haplotype, only plays a modulatory role in determining the frequency and severity of spontaneous autoimmune thyroiditis, while the presence of certain non-MHC associated genes is a absolute prerequisite for the emergence of the disease. The latter is also true for the genetically determined target organ susceptibility, while hormonal factors, notably sex-steroids and glucocorticoids, again only have a facultative, modulatory effect. Only if an appropriate genetic constellation concerning the non-MHC encoded aberrant immunological function and genes coding for the susceptibility of the thyroid gland for the autoimmune process is present, severe autoimmune thyroids develops.

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