天津医药

天津医药 ›› 2015, Vol. 43 ›› Issue (12): 1460-1463.doi: 10.11958/j.issn.0253-9896.2015.12.031

• 综述 • 上一篇    下一篇

CD38、CD138、IgG4在胆道闭锁发病中作用的研究进展

高婷1，詹江华2△   

  1. 1天津医科大学研究生院（邮编300070）；2天津市儿童医院外科
  • 收稿日期:2015-07-13 修回日期:2015-08-12 出版日期:2015-12-15 发布日期:2015-12-11
  • 通讯作者: △通讯作者E-mail: zhanjianghuatj@163.com E-mail:zhanjianghuatj@163.com
  • 作者简介:高婷（1989），女，硕士在读，主要从事胆道闭锁等相关研究

Current research in roles of CD38,CD138 and IgG4 in the pathogenesis of biliary atresia

GAO Ting1, ZHAN Jianghua2△   

  1. 1 Graduate School of Tianjin Medical University, Tianjin 300070, China; 2 Tianjin Children′s Hospital
  • Received:2015-07-13 Revised:2015-08-12 Published:2015-12-15 Online:2015-12-11
  • Contact: △Corresponding Author E-mail：zhanjianghuatj@163.com E-mail:zhanjianghuatj@163.com

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摘要： 胆道闭锁（biliary atresia,BA）是婴儿期最严重的肝胆系统疾病之一，以肝内外胆管进行性炎症和纤维性梗阻为特征。目前BA 的病因并不明确，可能与遗传易感、病毒感染、免疫损伤有关，现多认为是多因素共同作用的结果。而在众多因素中,炎症免疫学说得到大多数学者支持。CD38、CD138、IgG4 在自身免疫性肝病中的作用机制已有相关文献报道，而BA 和其他的自身免疫性肝病有相似之处，在疾病进展过程中均有炎症免疫反应，对疾病的发生发展起着不可代替的作用，因此，本文就CD38、CD138、IgG4在BA 炎症免疫中的作用进行综述。

关键词: 胆道闭锁；抗原, CD38, 多配体蛋白聚糖1, 免疫球蛋白G, 肝炎, 自身免疫性, CD138, IgG4

Abstract: Biliary atresia (BA) is one of the most serious pediatric surgical digestive system diseases with progressive liv⁃ er bile duct inflammation and fibrous obstruction. Currently, the etiology of BA is not clear. It may be associated with genetic predisposition, viral infections and immune injury. Now many scholars believe that it was resulted from multiple factors. Among them, the theory of immune-inflammatory is supported by most scholars. Now the mechanisms of CD38, CD138 and IgG4 in autoimmune liver disease were reported in literature. BA and other autoimmune liver diseases are similar in terms that both inflammatory and immune responses plays irreplaceable role during disease development. Therefore, this article briefly review the role of CD38, CD138 and IgG4 in the inflammation-immunity of BA.

Key words: biliary atresia, antigens, CD38, syndecan-1, immunoglobulin G, hepatitis, autoimmune, CD138, IgG4