Jackson R, McNicol A M, Farquharson M, Foulis A K
University Department of Pathology, Glasgow Royal Infirmary, U.K.
J Pathol. 1988 Jun;155(2):113-20. doi: 10.1002/path.1711550207.
It has been proposed that aberrant expression of class II major histocompatibility complex (MHC) molecules by target cells may be an initiating factor in some forms of organ specific autoimmunity. This hypothesis was tested in relation to the autoimmune form of Addison's disease by studying autopsy adrenal glands from eight patients who had died of recent onset idiopathic Addison's disease. Using an immunohistochemical technique, class II MHC expression was found in a minority of adrenal cortical cells in the zona reticularis in 25 normal and four hyperplastic glands, while in Addison's disease almost all residual cortical cells expressed class II MHC. Three tuberculous adrenals showed increased staining of cortical cells around areas of chronic inflammation. It is concluded that since adrenal cortical cells of the normal gland express class II MHC, aberrant expression of this product cannot be invoked as an initiating mechanism in autoimmune adrenalitis. The increased cortical expression of class II MHC seen in idiopathic Addison's disease and tuberculosis may be due to local release of lymphokines by inflammatory cells.
有观点认为,靶细胞中II类主要组织相容性复合体(MHC)分子的异常表达可能是某些形式的器官特异性自身免疫的起始因素。通过研究8例近期发病的特发性Addison病死亡患者的尸检肾上腺,对这一假说与Addison病的自身免疫形式进行了验证。采用免疫组织化学技术,在25个正常肾上腺和4个增生肾上腺的网状带少数肾上腺皮质细胞中发现了II类MHC表达,而在Addison病中,几乎所有残留的皮质细胞都表达II类MHC。3个结核性肾上腺在慢性炎症区域周围的皮质细胞染色增加。得出的结论是,由于正常肾上腺的皮质细胞表达II类MHC,因此不能将该产物的异常表达作为自身免疫性肾上腺炎的起始机制。在特发性Addison病和结核病中观察到的II类MHC皮质表达增加可能是由于炎症细胞局部释放淋巴因子所致。