自身免疫性疾病的多因素发病机制。

The multi-factorial pathogenesis of autoimmune disease.

作者信息

Wick G, Krömer G, Neu N, Fässler R, Ziemiecki A, Müller R G, Ginzel M, Béládi I, Kühr T, Hála K

机构信息

Institute for General and Experimental Pathology, University of Innsbruck, Medical School, Austria.

出版信息

Immunol Lett. 1987 Dec;16(3-4):249-57. doi: 10.1016/0165-2478(87)90154-4.

DOI:10.1016/0165-2478(87)90154-4

PMID:3127334

Abstract

Development of organ-specific autoimmune diseases depends on both an abnormal immune regulation and a genetically determined primary susceptibility of the target organ to the autoimmune attack. In addition to the essential genetically determined prerequisites there are also facultative, modulating factors that influence the outcome of an autoimmune disease. This concept is exemplified in the Obese strain (OS) chicken model which develops a spontaneous autoimmune thyroiditis closely resembling human Hashimoto disease. Three modulating factors are specifically addressed, viz. (a) the lower threshold of OS thyroid epithelial cells for the gamma-interferon-induced MHC class II antigen expression as compared to normal controls, (b) the decreased glucocorticoid tonus of the OS and (c) the presence of a new endogenous virus (ev 22) locus in the OS that has so far not been found in any normal strain and which seems to influence the glucocorticoid-mediated immunoregulatory process.

摘要

器官特异性自身免疫性疾病的发生既依赖于异常的免疫调节，也依赖于目标器官对自身免疫攻击的遗传决定的原发性易感性。除了基本的遗传决定因素外，还有一些影响自身免疫性疾病结局的兼性调节因素。肥胖品系（OS）鸡模型就例证了这一概念，该模型会发生一种与人类桥本氏病极为相似的自发性自身免疫性甲状腺炎。具体探讨了三个调节因素，即：（a）与正常对照相比，OS甲状腺上皮细胞对γ干扰素诱导的MHC II类抗原表达的阈值较低；（b）OS的糖皮质激素张力降低；（c）OS中存在一个新的内源性病毒（ev 22）位点，该位点迄今在任何正常品系中均未发现，且似乎影响糖皮质激素介导的免疫调节过程。