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

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
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

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
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

More Information
  • 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。
  • [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
  • 加载中
计量
  • 文章访问数:  47
  • HTML全文浏览量:  15
  • PDF下载量:  12
  • 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

    【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!