Increased expression of nuclear envelope gp210 antigen in small bile ducts in primary biliary cirrhosis
Increased expression of nuclear envelope gp210 antigen in small bile ducts in primary biliary cirrhosis
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DOI：
10.1016/j.jaut.2005.10.007
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发表时间：
2006-03-01
影响因子：
12.8
通讯作者：
Ishibashi, H
中科院分区：
文献类型：
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作者：
Nakamura, M;Takii, Y;Ishibashi, H
对核膜gp210抗原的持续抗体应答表明一组原发性胆汁性肝硬化（PBC）患者进展为终末期肝衰竭的风险较高。为了解决这一问题，我们使用特异性针对gp210抗原的单克隆抗体对PBC患者的肝穿刺活检标本中gp210抗原的表达进行了免疫组化研究。自身免疫性肝炎（AIH）、慢性乙型病毒性肝炎（CHB）和丙型病毒性肝炎（CHC）患者的标本作为疾病对照。几乎所有PBC标本的小胆管上皮细胞核被膜上gp210抗原表达均明显增强。正常肝小胆管BEC不表达gp210抗原，而AM、CHC和CHB的gp210抗原表达较弱。此外，gp210在小胆管BEC中的表达程度与PBC的门静脉炎症、界面性肝炎和小叶炎症呈正相关。这些结果表明，gp210在小胆管中的表达增加，这可能与炎症对BEC的损伤有关，可能涉及对gp210的自身免疫反应，导致PBC进展为终末期肝功能衰竭。(c)2005爱思唯尔有限公司保留所有权利。
The sustained antibody response to nuclear envelope gp210 antigen indicates a group of primary biliary cirrhosis (PBC) patients at high risk for the progression to end-stage hepatic failure. To address this issue, we immunohistochemically studied the expression of gp210 antigen in needle liver biopsy specimens from PBC patients using a monoclonal antibody specific for gp210 antigen. The specimens from autoimmune hepatitis (AIH), chronic viral hepatitis B (CHB) and C (CHC) patients served as disease controls. The expression of gp210 antigen was apparently increased on the nuclear envelope of biliary epithelial cells (BECs) of small bile ducts in almost all specimens from PBC. In contrast, the expression of gp210 antigen was negative in BECs of small bile ducts in normal liver, while relatively weak anti-gp210 immunostaining was observed in AM, CHC and CHB. In addition, the degree of gp210 expression in BECs of small bile ducts was positively correlated to that of portal inflammation, interface hepatitis and lobular inflammation in PBC. These results indicate that the increased expression of gp210 in small bile ducts, which is probably associated with damage to BECs by inflammation, is possibly involved in autoimmune response to gp210 leading to the progression to end-stage hepatic failure in PBC. (c) 2005 Elsevier Ltd. All rights reserved.