Characterization of biliary intra‐epithelial lymphocytes at different anatomical levels of intrahepatic bile ducts under normal and pathological conditions: Numbers of CD4+CD28– intra‐epithelial lymphocytes are increased in primary biliary cirrhosis
Characterization of biliary intra‐epithelial lymphocytes at different anatomical levels of intrahepatic bile ducts under normal and pathological conditions: Numbers of CD4+CD28– intra‐epithelial lymphocytes are increased in primary biliary cirrhosis
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DOI：
10.1111/j.1440-1827.2006.01913.x
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发表时间：
2006-01
影响因子：
2.2
通讯作者：
K. Isse;K. Harada;Yasunori Sato;Y. Nakanuma
中科院分区：
文献类型：
--
作者：
K. Isse;K. Harada;Yasunori Sato;Y. Nakanuma
在正常和病变肝脏，特别是原发性胆汁性肝硬化（PBC）中，检查了上皮内淋巴细胞沿着肝内胆管树（bIEL）的分布及其密度和表型。应用免疫组化法检测了28例正常肝、13例慢性病毒性肝炎（CVH）、13例PBC、5例原发性硬化性胆管炎（PSC）、7例肝外胆管梗阻（EBO）和16例肝内胆管结石患者的bIEL。在正常肝脏中，与小叶间胆管相比，大胆管和间隔胆管的bIEL相对致密。其中大部分CD 3和CD 8阳性，少数CD 4、CD 20和CD 57阳性。在CVH、PSC和EBO中，bIEL的分布、表型和密度均与正常肝无差异。在肝内胆管结石中，含结石导管中的CD 8 +bIEL数量增加。在PBC中，CD 4 + CD 28-bIEL的数量在受损的小叶间导管中显著增加，据报道，CD 4 + CD 28-bIEL是导致自身免疫性疾病中靶组织破坏的原因。结论：CD 3 + CD 8 +bIEL可能参与正常肝脏和CVH、PSC和EBO肝内胆管的免疫稳态。PBC和肝内胆管结石患者bIEL的分布和表型改变可能反映了它们参与了胆道病变。PBC受损胆管中CD 4 + CD 28-bIEL升高可能与免疫介导的胆管损伤有关。
Distribution of intra‐epithelial lymphocytes along intrahepatic biliary tree (bIEL), and their density and phenotype were examined in normal and diseased livers, particularly in primary biliary cirrhosis (PBC). Immunohistochemically, bIEL were examined in 28 normal livers, 13 cases of chronic viral hepatitis (CVH), 13 cases of PBC, five cases of primary sclerosing cholangitis (PSC), seven cases of extrahepatic biliary obstruction (EBO), and 16 hepatolithiatic livers. In normal livers, bIEL were relatively dense at large and septal bile ducts compared to interlobular ducts. Most of them were positive for CD3 and CD8, while a few were positive for CD4, CD20 and CD57. In CVH, PSC and EBO, neither distribution, phenotype nor density of bIEL differed from normal liver. In hepatolithiasis, numbers of CD8+bIEL were increased in stone‐containing ducts. In PBC, numbers of CD4+CD28–bIEL, which are reportedly responsible for target tissue destruction in autoimmune diseases, were markedly increased in damaged interlobular ducts. In conclusion, CD3+CD8+bIEL may be involved in immune homeostasis of intrahepatic bile ducts in normal livers and in CVH, PSC and EBO. Altered distribution and phenotypes of bIEL in PBC and hepatolithiasis may reflect their participation in biliary lesions. Increased CD4+CD28–bIEL in damaged bile ducts of PBC may be related to immune‐mediated biliary damage.