邮件订阅 RSS

留言板

尊敬的读者、作者、审稿人, 关于本刊的投稿、审稿、编辑和出版的任何问题, 您可以本页添加留言。我们将尽快给您答复。谢谢您的支持!

姓名
邮箱
手机号码
标题
留言内容
验证码

CD8+ T淋巴细胞在原发性胆汁性胆管炎发病机制中的调控与作用

陶葸茜,  王立,  张奉春

downloadPDF
文章导航 > 协和医学杂志  > 2017 >  8(4-5): 278-282
陶葸茜, 王立, 张奉春. CD8+ T淋巴细胞在原发性胆汁性胆管炎发病机制中的调控与作用[J]. 协和医学杂志, 2017, 8(4-5): 278-282. doi: 10.3969/j.issn.1674-9081.2017.05.016
引用本文: 陶葸茜, 王立, 张奉春. CD8+ T淋巴细胞在原发性胆汁性胆管炎发病机制中的调控与作用[J]. 协和医学杂志, 2017, 8(4-5): 278-282. doi: 10.3969/j.issn.1674-9081.2017.05.016
shu
Xi-xi TAO, Li WANG, Feng-chun ZHANG. CD8+ T Cells in the Pathogenesis of Primary Biliary Cholangitis[J]. Medical Journal of Peking Union Medical College Hospital, 2017, 8(4-5): 278-282. doi: 10.3969/j.issn.1674-9081.2017.05.016
Citation: Xi-xi TAO, Li WANG, Feng-chun ZHANG. CD8+ T Cells in the Pathogenesis of Primary Biliary Cholangitis[J]. Medical Journal of Peking Union Medical College Hospital, 2017, 8(4-5): 278-282. doi: 10.3969/j.issn.1674-9081.2017.05.016
shu

CD8+ T淋巴细胞在原发性胆汁性胆管炎发病机制中的调控与作用

doi: 10.3969/j.issn.1674-9081.2017.05.016
  • 1.

    中国医学科学院 北京协和医学院 北京协和医院 风湿免疫科, 北京 100730

  • 2.

    中国医学科学院 北京协和医学院 北京协和医院 超声医学科, 北京 100730

基金项目: 

国家自然科学基金面上项目 81571594

国家自然科学基金青年项目 81501414

国家自然科学基金青年项目 81501410

国家自然科学基金青年项目 81501413

首都卫生发展科研专项青年项目 2016-4-40111

详细信息
    通讯作者:

    王立  电话:010-69158770,E-mail:wangli2221@sina.com

  • 中图分类号: R575.7;R392.3

CD8+ T Cells in the Pathogenesis of Primary Biliary Cholangitis

  • 1.

    Department of Rheumatology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100730, China

  • 2.

    Department of Ultrasound, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100730, China

More Information

    摘要
  • 摘要: 原发性胆汁性胆管炎(primary biliary cholangitis, PBC)是一种以肝脏损害为主要表现的自身免疫性疾病, 其发病机制目前尚不明确, 可能与多种因素相关。其中, 在PBC的免疫功能紊乱中, CD8+ T淋巴细胞介导的细胞免疫有重要作用, 与PBC患者肝脏胆管上皮细胞受损有关。本文主要讨论CD8+ T细胞在PBC发病机制中的调控及该群细胞对PBC肝脏的损害作用。
    Abstract: Primary biliary cholangitis(PBC) is an autoimmune disease characterized by the liver damage. The pathogenesis of PBC is not fully understood currently, and many factors are involved. The cellular immunity mediated by CD8+ T cells plays an important role in the immune dysregulation of PBC, which is related to the injury of biliary epithelial cells. This review is mainly about the regulation of CD8+ T cells that involves several mechanisms, and the function of this group of cells in the liver damage of PBC patients.
    • HTML全文
    • 参考文献(26)
  • [1] Momah N, Lindor KD. Primary biliary cirrhosis in adults[J]. Expert Rev Gastroenterol Hepatol, 2014, 8:427-433. doi:  10.1586/17474124.2014.888950
    [2] Carey EJ, Ali AH, Lindor KD. Primary biliary cirrhosis[J]. Lancet, 2015, 386:1565-1575. doi:  10.1016/S0140-6736(15)00154-3
    [3] Gravano DM, Hoyer KK. Promotion and prevention of autoimmune disease by CD8+ T cells[J]. J Autoimmun, 2013, 45:68-79. doi:  10.1016/j.jaut.2013.06.004
    [4] Kita H, Matsumura S, He XS, et al. Quantitative and functional analysis of PDC-E2-specific autoreactive cytotoxic T lymphocytes in primary biliary cirrhosis[J]. J Clin Invest, 2002, 109:1231-1240. doi:  10.1172/JCI0214698
    [5] Gershwin ME, Mackay IR, Sturgess A, et al. Identification and specificity of a cDNA encoding the 70 kd mitochondrial antigen recognized in primary biliary cirrhosis[J]. J Immunol, 1987, 138:3525-3531. http://pmj.bmj.com/cgi/ijlink?linkType=ABST&journalCode=jimmunol&resid=138/10/3525
    [6] Kita H, Lian ZX, Van De Water J, et al. Identification of HLA-A2-restricted CD8(+) cytotoxic T cell responses in primary biliary cirrhosis:T cell activation is augmented by immune complexes cross-presented by dendritic cells[J]. J Exp Med, 2002, 195:113-123. doi:  10.1084/jem.20010956
    [7] Migliaccio C, Van De Water J, Ansari AA, et al. Heterogeneous response of antimitochondrial autoantibodies and bile duct apical staining monoclonal antibodies to pyruvate dehydrogenase complex E2:the molecule versus the mimic[J]. Hepatology, 2001, 33:792-801. doi:  10.1053/jhep.2001.23783
    [8] Kita H. Autoreactive CD8-specific T-cell response in primary biliary cirrhosis[J]. Hepatol Res, 2007, 37:S402-S405. doi:  10.1111/j.1872-034X.2007.00238.x
    [9] Kita H, Matsumura S, He XS, et al. Analysis of TCR antagonism and molecular mimicry of an HLA-A0201-restricted CTL epitope in primary biliary cirrhosis[J]. Hepatology, 2002, 36:918-926. doi:  10.1053/jhep.2002.35616
    [10] Crispe IN. The liver as a lymphoid organ[J]. Annu Rev Immunol, 2009, 27:147-163. doi:  10.1146/annurev.immunol.021908.132629
    [11] Crispe IN, Giannandrea M, Klein I, et al. Cellular and molecular mechanisms of liver tolerance[J]. Immunol Rev, 2006, 213:101-118. doi:  10.1111/j.1600-065X.2006.00435.x
    [12] Shimoda S, Harada K, Niiro H, et al. CX3CL1(fractalkine):a signpost for biliary inflammation in primary biliary cirrhosis[J]. Hepatology, 2010, 51:567-575. doi:  10.1002/hep.23318
    [13] Sasaki M, Miyakoshi M, Sato Y, et al. Chemokine-chemokine receptor CCL2-CCR2 and CX3CL1-CX3CR1 axis may play a role in the aggravated inflammation in primary biliary cirrhosis[J]. Dig Dis Sci, 2014, 59:358-364. doi:  10.1007/s10620-013-2920-6
    [14] Groom JR, Luster AD. CXCR3 in T cell function[J]. Exp Cell Res, 2011, 317:620-631. doi:  10.1016/j.yexcr.2010.12.017
    [15] Ma HD, Ma WT, Liu QZ, et al. Chemokine receptor CXCR3 deficiency exacerbates murine autoimmune cholangitis by promoting pathogenic CD8+ T cell activation[J]. J Autoimmun, 2017, 78:19-28. doi:  10.1016/j.jaut.2016.12.012
    [16] Yao Y, Yang W, Yang YQ, et al. Distinct from its canonical effects, deletion of IL-12p40 induces cholangitis and fibrosis in interleukin-2Rα-/- mice[J]. J Autoimmun, 2014, 51:99-108. doi:  10.1016/j.jaut.2014.02.009
    [17] Ouyang W, Oh SA, Ma Q, et al. TGF-β Cytokine Signaling Promotes CD8(+) T Cell Development and Low-affinity CD4(+) T Cell Homeostasis by Regulation of Interleukin-7 Receptor-α Expression[J]. Immunity, 2013, 39:335-346. doi:  10.1016/j.immuni.2013.07.016
    [18] Gorelik L, Flavell RA. Abrogation of TGFbeta signaling in T cells leads to spontaneous T cell differentiation and autoimmune disease[J]. Immunity, 2000, 12:171-181. doi:  10.1016/S1074-7613(00)80170-3
    [19] Arsenijevic A, Milovanovic M, Milovanovic J, et al. Deletion of Galectin-3 enhances xenobiotic induced murine primary biliary cholangitis by facilitating apoptosis of BECs and release of autoantigens[J]. Sci Rep, 2016, 6:23348. doi:  10.1038/srep23348
    [20] Lleo A, Bian Z, Zhang H, et al. Quantitation of the rank-rankl axis in primary biliary cholangitis[J]. PLoS One, 2016, 11:e0159612. doi:  10.1371/journal.pone.0159612
    [21] Yang GX, Lian ZX, Chuang YH, et al. Adoptive transfer of CD8(+) T cells from transforming growth factor beta receptor type Ⅱ(dominant negative form) induces autoimmune cholangitis in mice[J]. Hepatology, 2008, 47:1974-1982. doi:  10.1002/hep.22226
    [22] Huang W, Kachapati K, Adams D, et al. Murine autoimmune cholangitis requires two hits:Cytotoxic KLRG1+ CD8 effector cells and defective T regulatory cells[J]. J Autoimmun, 2014, 50:123-134. doi:  10.1016/j.jaut.2014.01.034
    [23] Yang JB, Wang YH, Yang W, et al. Successful treatment of murine autoimmune cholangitis by parabiosis:Implications for hematopoietic therapy[J]. J Autoimmun, 2016, 66:108-117. doi:  10.1016/j.jaut.2015.09.002
    [24] Youngblood B, Oestreich KJ, Ha SJ, et al. Chronic virus infection enforces demethylation of the locus that encodes PD-1 in antigen-specific CD8(+) T cells[J]. Immunity, 2011, 35:400-412. doi:  10.1016/j.immuni.2011.06.015
    [25] Concepcion AR, Salas JT, Sáez E, et al. CD8+ T cells undergo activation and programmed death-1 repression in the liver of aged Ae2a, b-/- mice favoring autoimmune cholangitis[J]. Oncotarget, 2015, 6:28588-28606. doi:  10.18632/oncotarget.5665
    [26] Lleo A, Zhang W, Zhao M, et al. DNA methylation profiling of the X chromosome reveals an aberrant demethylation on CXCR3 promoter in primary biliary cirrhosis[J]. Clin Epigenetics, 2015, 7:61. doi:  10.1186/s13148-015-0098-9
    • 相关文章
    • 施引文献
  • 资源附件(0)
  • 加载中
WeChat 点击查看大图
计量
  • 文章访问数:  138
  • HTML全文浏览量:  36
  • PDF下载量:  14
  • 被引次数: 0
出版历程
  • 收稿日期:  2017-06-26
  • 刊出日期:  2017-09-30

目录

    /

    返回文章
    返回
    友情链接: 国家卫生健康委员会 北京协和医院 中国医学科学院 学术不端检测系统 国际知识资源总库 中国知网 术语在线 中国全科医学
    地址：北京市东城区帅府园1号 北京协和医院老楼7号楼
    3层302室 《协和医学杂志》编辑部
    电话：010-69154261/4262
    E - mail：medj@pumch.cn
    mjpumch@126.com
    期刊网站版权所有：《协和医学杂志》编辑部
    京ICP备 11002662

    本系统由 北京仁和汇智信息技术有限公司 开发    百度统计

    x 关闭 永久关闭

    【温馨提醒】近日，《协和医学杂志》编辑部接到作者反映，有多名不法人员冒充期刊编辑发送见刊通知，鼓动作者添加微信，从而骗取版面费的行为。特提醒您，本刊与作者联系的方式均为邮件通知或电话，稿件进度通知邮箱为：mjpumch@126.com，编辑部电话为：010-69154261，请提高警惕，谨防上当受骗！如有任何疑问，请致电编辑部核实。谢谢！