CAJ | 학술논문

目的:研究共刺激分子CD86和可诱导共刺激凶子(inducible co.stimulator,ICOS)在Crohn病(Crohndisease,CD)肠黏膜的表达及其病理意义.方法:采用免疫组织化学方法检测CD组(n=30)病变黏膜及相对正常黏膜共刺激分子CD86和ICOS的表达及CD4,CD8和CD20阳性表型的淋巴细胞分布,并与正常对照组(n=20)进行比较.结果:CD组病变黏膜固有层CD86~+和ICOS~+淋巴单核细胞数量显著高于CD组相对正常黏膜及正常对照组(q=9.23,P＜0.01和q=5.46,P＜0.01).同时,CD86及ICOS在肠上皮中亦有强表达,CD组高于对照组(H=24.93,P＜0.01和H=4.66,P＜0.01),而CD组内病变黏膜与相对正常黏膜的表达差异无统计学意义.另外,CD组病变黏膜的固有层、上皮内及小血管壁CD4~+T细胞和CD8~+T细胞数量均显著高于CD组相对正常黏膜及对照组(P＜0.05或P＜0.01).结论:CD病变组织中CD86~+和ICOS~+淋巴单核细胞数量显著增多及肠上皮阳性率显著提高,提示共刺激分子可能参与了CD细胞免疫的异常激活过程,CD肠上皮细胞可能作为非专职性抗原呈递细胞参与了该过程.
목적:연구공자격분자CD86화가유도공자격흉자(inducible co.stimulator,ICOS)재Crohn병(Crohndisease,CD)장점막적표체급기병리의의.방법:채용면역조직화학방법검측CD조(n=30)병변점막급상대정상점막공자격분자CD86화ICOS적표체급CD4,CD8화CD20양성표형적림파세포분포,병여정상대조조(n=20)진행비교.결과:CD조병변점막고유층CD86~+화ICOS~+림파단핵세포수량현저고우CD조상대정상점막급정상대조조(q=9.23,P＜0.01화q=5.46,P＜0.01).동시,CD86급ICOS재장상피중역유강표체,CD조고우대조조(H=24.93,P＜0.01화H=4.66,P＜0.01),이CD조내병변점막여상대정상점막적표체차이무통계학의의.령외,CD조병변점막적고유층、상피내급소혈관벽CD4~+T세포화CD8~+T세포수량균현저고우CD조상대정상점막급대조조(P＜0.05혹P＜0.01).결론:CD병변조직중CD86~+화ICOS~+림파단핵세포수량현저증다급장상피양성솔현저제고,제시공자격분자가능삼여료CD세포면역적이상격활과정,CD장상피세포가능작위비전직성항원정체세포삼여료해과정.
Objective: To investigate the expression of co-stimulatory molecule CD86 and inducible costimulator(ICOS) in the intestinal mucosa of Crohn disease (CD) and to exlpore its pathologic significance. Methods: Expression of co-stimulator CD86 and ICOS was examined by immunohistoehemistry on paraffin embedded tissue from patients with CD (30 cases) and normal controls (20 cases). The subsets of lamina propria mononuclear cells (LPMC) were also analysed via immunostaining for CD4, CD8 and CD20. Results: Increased amount of CD86 or ICOS positive LPMC was observed in the lesional area of CD when compared with the essentially normal area of CD and normal controls (q = 9. 23 ,P ＜0. 01 and q =5. 46 ,P＜0. 01). In addition, the expression of CD86 or ICOS was higher in intestinal epithelium of CD than that in normal controls (H = 24. 93, P＜0. 01 and H = 4. 66, P＜0. 01 ) , whereas no significant difference was seen between the diseased and the essentially normal area of CD. The amount of CD4 or CD8 positive lymphocytes in lamina propria, epithelium and small vascular walls was also significantly increased in CD than that in normal controls (P＜0. 05 or P＜0. 01). Conclusion: Increased amount of CD86 or ICOS positive LPMC and enterocytes in CD suggests that co-stimulatory molecules may play a role in the pathogenesis of CD. The enterocytes may act as non-specific antigen presenting cells in the process of cellular immunity activation in CD.