Pujol-Borrell R, Todd I, Londei M, Foulis A, Feldmann M, Bottazzo G F
Mol Biol Med. 1986 Apr;3(2):159-65.
"Inappropriate" expression of class II major histocompatibility complex (MHC) molecules by target cells has been found in all organ-specific autoimmune diseases so far examined for the presence of this phenomenon. These glycoproteins may have a functional role as class II+ thyrocytes are able to present both small fragments of foreign antigens and autoantigens to helper T cells. Interferon gamma is a likely modulator of MHC class II expression in the thyroid but other signals like thyroid-stimulating hormone seem to influence its action. By contrast, it appears that lymphokines are not involved in inducing the inappropriate MHC class II expression observed in situ in the pancreatic beta cells of diabetics. These data suggest that regulation of MHC class II expression is different in thyroid follicular cells from pancreatic beta cells, and that similar differences may be found in other cell types involved in autoimmune disease, thus reinforcing the concept of heterogeneity in the pathogenesis of organ-specific autoimmune disorders.
在目前所有针对该现象进行检测的器官特异性自身免疫性疾病中,均发现靶细胞存在II类主要组织相容性复合体(MHC)分子的“异常”表达。这些糖蛋白可能具有功能性作用,因为II类阳性甲状腺细胞能够将外来抗原和自身抗原的小片段呈递给辅助性T细胞。干扰素γ可能是甲状腺中MHC II类表达的调节因子,但其他信号(如促甲状腺激素)似乎会影响其作用。相比之下,细胞因子似乎并未参与诱导糖尿病患者胰腺β细胞原位观察到的MHC II类异常表达。这些数据表明,甲状腺滤泡细胞中MHC II类表达的调节与胰腺β细胞不同,并且在参与自身免疫性疾病的其他细胞类型中可能也存在类似差异,从而强化了器官特异性自身免疫性疾病发病机制中异质性的概念。