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作 者:徐德民[1] 蒋振斌[1] 周光华[1] 杨英珍[1] 熊丁丁[1]
机构地区:[1]上海医科大学附属中山医院心外科,200032
出 处:《中国临床医学杂志》1998年第3期138-139,共2页
摘 要:目的:探讨细胞介导的细胞毒作用在感染性心内膜炎发病中的意义。方法:应用免疫组织化学技术,对18例感染性心内膜炎患者和11例先天性心脏病患者的瓣膜(或心肌)标本的浸润淋巴细胞表型和穿孔素进行了检测。结果:在感染性心内膜炎瓣膜的浸润细胞中,发现有CD4+细胞10例,CD8+细胞14例,CD16+细胞12例;先心瓣膜(或心肌)仅2例有少量的CD4+细胞。穿孔素仅见于有CD8+/域CD16+细胞的14例感染性心内膜炎标本中。结论:细胞介导的细胞毒作用可能是感染性心内膜炎发病中的重要环节之一,穿孔素是由CD8+与CD16+等细胞释放的损伤瓣膜的主要效应分子。Objective: To clarify the role of cell- mediated cytotoxicity (CMC) in the etiology of infective endocarditis (IE).Materials and Methods: The valves or myocardium of 18 patients with IE and 11 patients with congenital heart diseases were studied through the phenotypes of infiltrating lymphocytes and perform by immunohistochemistry.Results: Results showed as follows: In the valves, 10, 14, 12 patients with IE, CD4+ , CD8+ , CD16+ cells were detected respectively and CD4 + cells were found in only two patients with congenital heart diseases; Perforin was only detected in the valves infiltrated by CD8 + and CD16 + cells of 4 patients with IE.Conclusion: The data indicateg that CMC may be one of the main factor in the efiologic cycle of IE. Perforin, as the effector molecule released by effector cell of CMC, may play a critical role in the valve damage occurring in IE.
分 类 号:R542.420.2[医药卫生—心血管疾病]
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