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Adhesion molecules intercellular adhesion molecule-1 (ICAM-1), ICAM-3 and B7 are not expressed by epithelium in normal or inflamed colon.

机译:在正常或发炎的结肠中,上皮不表达粘附分子细胞间粘附分子-1(ICAM-1),ICAM-3和B7。

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摘要

Adhesion molecules are involved in facilitating cell-mediated immune events. Because lymphocyte-epithelial cell interaction has been implicated in the pathogenesis of colonic inflammation, we analysed expression of a range of adhesion molecules on colonic epithelium in vitro and in vivo using flow cytometry, immunohistochemistry and in situ hybridization. Expression of ICAM-1 by cell lines HT29 and int407 was increased by proinflammatory cytokines interferon-gamma (IFN-gamma), tumour necrosis factor-alpha (TNF-alpha) and IL-1 but not by IL-6. Vascular cell adhesion molecule (VCAM) and E-selectin were not expressed. Immunohistochemistry using sections of inflamed colon from 16 patients with ulcerative colitis (UC), five patients with Crohn's disease (CD) and seven patients with normal colonoscopic biopsies, showed no expression of ICAM-1 on colonic epithelium. VCAM was seen in isolated lymphoid aggregates and E-selectin was expressed on endothelium. In situ hybridization showed no ICAM-1 or ICAM-3 mRNA in colonic epithelium. B7, the ligand for CD28, was not found on normal or inflamed colonic epithelium. The adhesion molecules ICAM-1, ICAM-3 and B7 are not involved in lymphocyte-epithelial cell interaction in the normal or inflamed colon. This may have implications for the development of T cell tolerance to intestinal luminal antigens.
机译:粘附分子参与促进细胞介导的免疫事件。由于淋巴细胞与上皮细胞的相互作用已经牵涉到结肠炎症的发病机理中,因此我们使用流式细胞仪,免疫组织化学和原位杂交技术分析了体外和体内结肠上皮细胞上一系列粘附分子的表达。促炎细胞因子干扰素-γ(IFN-γ),肿瘤坏死因子-α(TNF-α)和IL-1增加了细胞系HT29和int407的ICAM-1表达,但IL-6却没有。未表达血管细胞粘附分子(VCAM)和E-选择素。使用16例溃疡性结肠炎(UC),5例克罗恩氏病(CD)和7例结肠镜活检正常的患者发炎的结肠切片进行的免疫组织化学分析显示,结肠上皮细胞未表达ICAM-1。在分离的淋巴样聚集物中可见VCAM,并且在内皮上表达E-选择蛋白。原位杂交显示结肠上皮中没有ICAM-1或ICAM-3 mRNA。在正常或发炎的结肠上皮中未发现CD28的配体B7。粘附分子ICAM-1,ICAM-3和B7不参与正常结肠或发炎结肠中的淋巴细胞-上皮细胞相互作用。这可能对发展T细胞对肠腔抗原的耐受性有影响。

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