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作 者:卞兆连[1] 陈琳[1] 居林玲 苗琪[2] 马雄[2] 邵建国[1] 管海涛[1] BIAN Zhaolian CHEN Lin JU Linlin MIAO Qi MA Xiong SHAO Jianguo GUAN Haitao(Nantong Third People' s Hospital, Nantong Institute of Liver Disease, Jiangsu 226006 Division of Gastroenterology and Hepatology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai Institute of Digestive Disease)
机构地区:[1]南通市第三人民医院,南通市肝病研究所,江苏226006 [2]上海交通大学医学院附属仁济医院消化内科,上海市消化疾病研究所
出 处:《交通医学》2016年第4期307-310,共4页Medical Journal of Communications
基 金:南通市科技局资助项目(MS22015105,HS2014061,BK2014073);江苏省科技厅资助项目(BK2016420)
摘 要:目的:研究原发性胆汁性胆管炎(primary biliary cholangitis,PBC)中发生CD8+细胞毒性T细胞(cytotoxic T lymphocyte,CTL)穿入现象及其意义。方法:收集53例PBC患者肝穿刺标本,采用H&E染色和免疫荧光染色方法,在光学显微镜和激光共聚焦显微镜下观察PBC肝组织中CTL的穿入及穿入宿主细胞的类型,并分析与病程的关系。结果:53例PBC患者中10例(18.9%)发生淋巴细胞穿入肝细胞,15例(28.3%)发生淋巴细胞穿入胆管上皮,仅1例患者同时存在淋巴细胞穿入肝细胞和胆管上皮细胞。免疫荧光染色证实穿入的淋巴细胞是CD8阳性细胞毒性T细胞(CTL)。早期PBC患者中4例(22.2%)、晚期PBC患者中6例(17.1%)发生CTL穿入肝细胞,两组差异无统计学意义(P>0.05)。早期PBC患者中9例(50.0%)、晚期PBC患者中6例(17.1%)发生CTL穿入胆管上皮,两组差异有统计学意义(Z=2.52,P<0.05)。结论:在PBC肝组织中,CTL可穿入肝细胞和胆管上皮细胞,CTL穿入胆管上皮细胞并导致其发生凋亡可能是PBC发病过程中胆管损伤的机制之一。Objective:To explore the features of CD8 positive cytotoxic T lymphocytes (CTL) emperipolesis and its correlation with course of disease in primary biliary eholangitis (PBC). Methods:H&E staining was used to determine the phenotype of emperipolesis in PBC. In immunofluorescence, CK8/18 was the marker of hepatoeytes, while CK7 was used to mark cholangiocyte, and CD8 was the marker of CTL; Phenotypes of emperipolesis were observed under optical and laser confocal microscopes; And analyzed the correlation between emperipolesis and disease progression. Results :Two kinds of emperipolesis were observed in PBC, one is 'CTL into hepatocyte', another is 'CTL into cholangioeyte'. Negative correla- tion between 'CTL into cholangiocyte' and course of disease was found. 'CTL entry into cholangiocyte' lead to apoptosis of cholangioeyte. Conclusion:Both 'CTL into hepatocyte' and 'CTL into cholangiocyte'were observed in PBC, and apop- tosis of cholangiocyte induced by ' CTL into cholangiocyte' may be a mechanism of bile duct damage in PBC.
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