Jewell D P, Patel C
Scand J Gastroenterol Suppl. 1985;114:119-26. doi: 10.3109/00365528509093772.
Although the aetiology of ulcerative colitis and Crohn's disease remain unknown, immunological effector mechanisms become activated within the inflamed mucosa and may be responsible for the pathogenesis of chronic disease. There is an increased production of immunoglobulin within the mucosa, some of which has specificity for bacterial antigens, and complement activation occurs during exacerbation of the disease. Lymphocytes isolated from peripheral blood, or from the intestinal mucosa, are cytotoxic to colonic epithelial cells in vitro; a reaction which can be modulated by serum factors and bacterial antigens. Within the mucosa, there are increased populations of T lymphocytes although there is no change in the ratio of helper- to suppressor-cells as defined by phenotype. Studies of immunoregulatory control have shown that there may be alterations in the modulation of the local immune response, especially during active disease, although it is not clear whether these changes are primary or merely secondary to inflammation. It is posulated that many of the humoral and cellular responses to gut-associated antigens occur as a result of increased antigen absorption, increased presentation of antigen to the immune system due to the expression of Class II antigens by the inflamed epithelium and altered immuno-regulatory control.
尽管溃疡性结肠炎和克罗恩病的病因尚不清楚，但免疫效应机制在炎症黏膜内被激活，可能是慢性病发病机制的原因。黏膜内免疫球蛋白产生增加，其中一些对细菌抗原有特异性，并且在疾病加重期间发生补体激活。从外周血或肠黏膜分离的淋巴细胞在体外对结肠上皮细胞具有细胞毒性；这种反应可被血清因子和细菌抗原调节。在黏膜内，T淋巴细胞数量增加，尽管根据表型定义的辅助性T细胞与抑制性T细胞的比例没有变化。免疫调节控制的研究表明，局部免疫反应的调节可能存在改变，尤其是在疾病活动期，尽管尚不清楚这些变化是原发性的还是仅仅继发于炎症。据推测，对肠道相关抗原的许多体液和细胞反应是由于抗原吸收增加、炎症上皮细胞表达II类抗原导致抗原向免疫系统的呈递增加以及免疫调节控制改变而发生的。
