中华病理学杂志
中華病理學雜誌
중화병이학잡지
Chinese Journal of Pathology
2010年
1期
19-24
,共6页
李方%陈阿静%杜鹃%张燕%宫恩聪%石雪迎
李方%陳阿靜%杜鵑%張燕%宮恩聰%石雪迎
리방%진아정%두견%장연%궁은총%석설영
结肠炎%溃疡性%淋巴细胞亚群%共刺激因子
結腸炎%潰瘍性%淋巴細胞亞群%共刺激因子
결장염%궤양성%림파세포아군%공자격인자
Colitis,ulcerative%Lymphocyte subsets%Co-stimulators
目的 探讨共刺激因子及淋巴细胞亚型与溃疡性结肠炎活动性的关系,以及在肠黏膜中的分布特征及其与溃疡性结肠炎发病的关系.方法 采用免疫组织化学EnVision法检测溃疡性结肠炎活动期(64例)、缓解期(51例)及正常结肠黏膜(20例)石蜡标本中共刺激因子CD86和可诱导共刺激因子(ICOS)的表达及分布;检测9例溃疡性结肠炎患者(7例活动期,2例缓解期)及5例正常对照结肠黏膜的冷冻标本中共刺激因子CD28的表达及分布.同时检测CD4、CD8和CD20阳性淋巴细胞在肠黏膜中的分布,分析其与共刺激因子表达间的关系.结果 共刺激因子CD86在固有膜淋巴单核细胞及肠上皮细胞中的表达为活动期>缓解期>对照组(P<0.05或P<0.01);而ICOS在固有膜淋巴单核细胞表达为活动期高于缓解期及对照组,ICOS在肠上皮细胞表达为活动期高于缓解期(P<0.01).CD28表达为活动期高于缓解期及对照组(P<0.05或P<0.01).固有膜间质、上皮细胞问及小血管壁CD4~+辅助性T淋巴细胞和CD8~+细胞毒性T淋巴细胞的数量、CD4/CD8比值,以及CD20~+ B淋巴细胞数量均为活动期高于缓解期及对照组(P<0.01).结论 共刺激因子CD86、ICOS在溃疡性结肠炎肠上皮细胞和固有膜淋巴单核细胞中存在表达上调现象,提示共刺激因子的异常表达可能参与了溃疡性结肠炎发病过程中细胞免疫和体液免疫的过度激活.
目的 探討共刺激因子及淋巴細胞亞型與潰瘍性結腸炎活動性的關繫,以及在腸黏膜中的分佈特徵及其與潰瘍性結腸炎髮病的關繫.方法 採用免疫組織化學EnVision法檢測潰瘍性結腸炎活動期(64例)、緩解期(51例)及正常結腸黏膜(20例)石蠟標本中共刺激因子CD86和可誘導共刺激因子(ICOS)的錶達及分佈;檢測9例潰瘍性結腸炎患者(7例活動期,2例緩解期)及5例正常對照結腸黏膜的冷凍標本中共刺激因子CD28的錶達及分佈.同時檢測CD4、CD8和CD20暘性淋巴細胞在腸黏膜中的分佈,分析其與共刺激因子錶達間的關繫.結果 共刺激因子CD86在固有膜淋巴單覈細胞及腸上皮細胞中的錶達為活動期>緩解期>對照組(P<0.05或P<0.01);而ICOS在固有膜淋巴單覈細胞錶達為活動期高于緩解期及對照組,ICOS在腸上皮細胞錶達為活動期高于緩解期(P<0.01).CD28錶達為活動期高于緩解期及對照組(P<0.05或P<0.01).固有膜間質、上皮細胞問及小血管壁CD4~+輔助性T淋巴細胞和CD8~+細胞毒性T淋巴細胞的數量、CD4/CD8比值,以及CD20~+ B淋巴細胞數量均為活動期高于緩解期及對照組(P<0.01).結論 共刺激因子CD86、ICOS在潰瘍性結腸炎腸上皮細胞和固有膜淋巴單覈細胞中存在錶達上調現象,提示共刺激因子的異常錶達可能參與瞭潰瘍性結腸炎髮病過程中細胞免疫和體液免疫的過度激活.
목적 탐토공자격인자급림파세포아형여궤양성결장염활동성적관계,이급재장점막중적분포특정급기여궤양성결장염발병적관계.방법 채용면역조직화학EnVision법검측궤양성결장염활동기(64례)、완해기(51례)급정상결장점막(20례)석사표본중공자격인자CD86화가유도공자격인자(ICOS)적표체급분포;검측9례궤양성결장염환자(7례활동기,2례완해기)급5례정상대조결장점막적냉동표본중공자격인자CD28적표체급분포.동시검측CD4、CD8화CD20양성림파세포재장점막중적분포,분석기여공자격인자표체간적관계.결과 공자격인자CD86재고유막림파단핵세포급장상피세포중적표체위활동기>완해기>대조조(P<0.05혹P<0.01);이ICOS재고유막림파단핵세포표체위활동기고우완해기급대조조,ICOS재장상피세포표체위활동기고우완해기(P<0.01).CD28표체위활동기고우완해기급대조조(P<0.05혹P<0.01).고유막간질、상피세포문급소혈관벽CD4~+보조성T림파세포화CD8~+세포독성T림파세포적수량、CD4/CD8비치,이급CD20~+ B림파세포수량균위활동기고우완해기급대조조(P<0.01).결론 공자격인자CD86、ICOS재궤양성결장염장상피세포화고유막림파단핵세포중존재표체상조현상,제시공자격인자적이상표체가능삼여료궤양성결장염발병과정중세포면역화체액면역적과도격활.
Objective To study the expression and localization of co-stimulators in the mueosa of patients with ulcerative colitis ( UC) , and to explore its role in the pathogenesis of UC. Methods Expression of co-stimulators CD86 and inducible co-stimulator (ICOS) was studied by immunohistochemistry on paraffin-embedded mucosal tissue from patients with active UC (64 cases) , inactive UC (51 cases) and normal controls (20 cases). Immunostaining for CD28 was also carried out on frozen fresh mucosal tissue sampled from patients with active UC (7 cases) , inactive UC (2 cases) and normal controls (5 cases). In addition, expression of CD4, CD8 and CD20 were also examined. Results In active UC, increased expression of CD86 was not only observed in lamina propria mononuclear cells but also in the intestinal epithelial cells, as compared with inactive UC and the normal controls (P < 0. 01 ) . Increased ICOS expression in lamina propria mononuclear cells was detected in active UC, as compared with inactive UC and the normal controls (P<0. 01). Increased ICOS expression in intestinal epithelial cells was also seen in active UC, as compared with that of inactive UC ( P < 0. 01 ). The expression of CD86 was higher in inactive UC than in the normal controls ( P < 0. 05 or P < 0. 01 ) . However, the expression of ICOS showed no statistically significant difference between inactive UC and normal controls. Increased expression of CD28 in active UC, compared with that in inactive UC and normal controls, was also noticed ( P < 0. 05 or P < 0. 01). The number of CD4 or CD8-positive intraepithelial lymphocytes and lymphocytes infiltrating in the lamina propria and small vessel walls was much higher in active UC than in inactive UC and normal controls ( P < 0. 01). Moreover, the ratio of CD4/CD8 was highest in active UC (P < 0. 01). The number of CD20-positive B lymphocytes in lamina propria was also higher in active UC than in inactive UC and normal controls (P < 0. 01). Conclusions In active UC, CD86 and ICOS were over-expressed in the intestinal epithelial cells and lamina propria mononuclear cells. The phenomenon suggests that abnormal expression of co-stimulators may contribute to the deregulation of acquired immune responses in UC.