Koretz K, Momburg F, Otto H F, Möller P
Institute of Pathology, Heidelberg University, West Germany.
Am J Pathol. 1987 Dec;129(3):493-502.
Changes were examined in the expression of Class I and II major histocompatibility complex (MHC) antigens by autochthonous cells of the terminal ileum affected by Crohn's disease. The study was based on the analysis of transmural specimens from terminal ileum segments obtained in the course of ileocolectomy for colon cancer and Crohn's disease. Serial sections were immunostained using monoclonal antibodies directed against monomorphic determinants of HLA-A,B,C, DR, DP, DQ, and the invariant chain (Ii) associated with Class II molecules. Compared with the normal state, the only change in Class I antigen expression occurring in Crohn's disease was the induction of HLA-A,B,C antigens in lymphatic endothelium. Changes in Class II antigen expression were more substantial. Enhancement of HLA-DR expression was found in enterocytes; DR induction was observed in glial cells of the visceral nervous plexus and in venular and venous endothelium. HLA-DP and DQ antigens were induced in enterocytes, glial cells, and capillary and venular endothelium, although this induction was restricted to areas of moderate or high inflammatory activity. The tissue distribution of Ii closely resembled that of HLA-DR, although this association was not strict: on the one hand, arterial endothelium contained low amounts of Ii in the absence of DR antigens; on the other hand, glial cells expressed Class II molecules in the absence of Ii. The extent of local enhancement/induction of MHC antigens was positively correlated with the local density of the cellular infiltrate. These data suggest that altered MHC antigen expression by autochthonous structures might be mediated by factors released from the lymphohistiocytic infiltrate, which is itself attracted by an unknown signal. In conjunction with an unknown antigen, the enhanced expression of Class II antigens might trigger an autoaggressive immune response.
研究了克罗恩病累及的回肠末端自身细胞中I类和II类主要组织相容性复合体（MHC）抗原的表达变化。该研究基于对因结肠癌和克罗恩病行回结肠切除术时获取的回肠末端节段透壁标本的分析。连续切片使用针对HLA - A、B、C、DR、DP、DQ单态决定簇以及与II类分子相关的恒定链（Ii）的单克隆抗体进行免疫染色。与正常状态相比，克罗恩病中I类抗原表达的唯一变化是淋巴管内皮细胞中HLA - A、B、C抗原的诱导。II类抗原表达的变化更为显著。在肠上皮细胞中发现HLA - DR表达增强；在内脏神经丛的神经胶质细胞以及小静脉和静脉内皮细胞中观察到DR诱导。HLA - DP和DQ抗原在肠上皮细胞、神经胶质细胞以及毛细血管和小静脉内皮细胞中被诱导，尽管这种诱导仅限于中度或高度炎症活动区域。Ii的组织分布与HLA - DR非常相似，尽管这种关联并不严格：一方面，动脉内皮细胞在没有DR抗原的情况下含有少量的Ii；另一方面，神经胶质细胞在没有Ii的情况下表达II类分子。MHC抗原局部增强/诱导的程度与细胞浸润的局部密度呈正相关。这些数据表明，自身结构中MHC抗原表达的改变可能由淋巴细胞 - 组织细胞浸润释放的因子介导，而这种浸润本身是由未知信号吸引的。与未知抗原一起，II类抗原的增强表达可能引发自身攻击性免疫反应。
