Hepatocyte lesions and cellular immune response in yellow fever infection
Hepatocyte lesions and cellular immune response in yellow fever infection
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DOI：
10.1016/j.trstmh.2006.02.019
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发表时间：
2007-02-01
影响因子：
2.2
通讯作者：
Duarte, Maria I. S.
中科院分区：
文献类型：
--
作者：
Quaresma, Juarez A. S.;Barros, Vera L. R. S.;Duarte, Maria I. S.
原位细胞免疫反应的研究对于了解不同的肝脏感染是非常重要的。在本研究中，分析了53例在丛林黄热病过程中死亡的患者通过内脏切开术获得的肝脏样本。经血清学、病毒分离和病毒特异性免疫组化证实。采用免疫组化方法检测细胞凋亡、CD 45 RO、CD 4、CD 8、CD 20、S100、CD 57和CD 68的表达。标记模式的定量分析表明，在门脉道和腺泡的中区区域的不同表型的明显优势。以T CD 4+淋巴细胞为主，同时存在T CD 8+淋巴细胞、自然杀伤细胞（CD 57）、巨噬细胞和抗原呈递细胞（S100）。炎症强度和肝损伤程度之间的不成比例可能是由于强烈的凋亡成分，这通常不会诱导炎症反应。本研究表明，尽管损伤和炎症之间的不成比例，细胞免疫反应在黄热病肝细胞损伤的发病机制中起着重要作用，可能是由于通过涉及MHC II和Fas受体和颗粒酶/穿孔素的激活机制的细胞溶解作用。(C)2006年皇家热带医学和卫生学会。由爱思唯尔有限公司出版。保留所有权利。
The study of the in-situ cellular immune response is very important for the understanding of different liver infections. In the present study, 53 liver samples obtained by viscerotomy from patients who died during the course of jungle yellow fever were analyzed. The diagnosis was confirmed by serology, viral isolation and virus-specific immunohistochemistry. The specimens were analyzed by immunohistochemistry using specific antibodies for apoptosis, CD45RO, CD4, CD8, CD20, S100, CD57 and CD68. Quantitative analysis of the labeling pattern showed a clear predominance of the different phenotypes in the portal tract and midzone region of the acini. There was a predominance of T CD4+ lymphocytes, accompanied by the presence of T CD8+ lymphocytes, natural killer cells (CD57), macrophages and antigen-presenting cells (S100). The disproportion between the intensity of inflammation and the degree of hepatic injury was probably due to the intense apoptotic component, which classically does not induce an inflammatory response. The present study demonstrates that, despite the disproportion between injury and inflammation, the cellular immune response plays an important role in the pathogenesis of the hepatocytic injury observed in yellow fever, probably as a result of cytolytic actions through mechanisms involving MHC II and the activation of Fas receptors and granzymes/perforins. (C) 2006 Royal Society of Tropical Medicine and Hygiene. Published by Elsevier Ltd. All rights reserved.