Kanzaki K, Mizuno M, Tsuji T
First Department of Internal Medicine, Okayama University Medical School, Japan.
Acta Med Okayama. 1991 Aug;45(4):249-56. doi: 10.18926/AMO/32164.
The immunologic mechanisms mediated by anticolon antibodies have been suggested for the injury of colonic mucosa in ulcerative colitis (UC). For the understanding of pathogenetic relevance of the anticolon antibody in UC, we examined the class and the subclass of the anticolon antibody reactive to rat colonic epithelial cells in sera from 10 patients with UC immunohistochemically by an indirect immunoperoxidase method. We also examined the distribution of the antigen recognized by the anticolon antibody by immunoelectron microscopy. The antibody reactive to the rat colonic epithelial cell was detected in 2 of the 10 patients, and the class and subclass of the antibody was mainly IgG2. The antigen recognized by the anticolon antibody was located on the apical membrane of the colonic epithelial cells and mucous substances of the goblet cells. These findings suggest that the anticolon antibody detected in this study is inadequate to cause the colonic mucosal injury by activating complements or mediating antibody-dependent cellular cytotoxicity. A potential pathogenetic role of the anticolon antibody in UC remains to be established.
抗结肠抗体介导的免疫机制被认为与溃疡性结肠炎(UC)结肠黏膜损伤有关。为了解抗结肠抗体在UC发病机制中的相关性,我们采用间接免疫过氧化物酶法,通过免疫组织化学检测了10例UC患者血清中与大鼠结肠上皮细胞反应的抗结肠抗体的类别和亚类。我们还通过免疫电子显微镜检查了抗结肠抗体识别的抗原分布。在10例患者中的2例检测到了与大鼠结肠上皮细胞反应的抗体,该抗体的类别和亚类主要为IgG2。抗结肠抗体识别的抗原位于结肠上皮细胞的顶端膜和杯状细胞的黏液物质上。这些发现表明,本研究中检测到的抗结肠抗体不足以通过激活补体或介导抗体依赖性细胞毒性来导致结肠黏膜损伤。抗结肠抗体在UC中的潜在致病作用仍有待确定。