中文English
ISSN 1001-5256 (Print)
ISSN 2097-3497 (Online)
CN 22-1108/R
Volume 37 Issue 4
Apr.  2021
Turn off MathJax
Article Contents

Role of Kupffer cells in the development and progression of primary biliary cholangitis

DOI: 10.3969/j.issn.1001-5256.2021.04.051
  • Received Date: 2020-10-08
  • Accepted Date: 2020-12-03
  • Published Date: 2021-04-20
  • The incidence rate of primary biliary cholangitis (PBC) is increasing year by year, but there is still no specific medicine at present and PBC has a complex pathogenesis. Kupffer cells, as the key cells involved in immunoregulation, play an important role in PBC. When hepatocytes are damaged, Kupffer cells will be activated and release a large amount of inflammatory cytokines and chemokines, which participate in the development and progression of PBC. This article briefly reviews the role of Kupffer cells in PBC, so as to provide a theoretical basis for Kupffer cells as a potential target for the treatment of PBC.

     

  • loading
  • [1]
    CAREY EJ, ALI AH, LINDOR KD. Primary biliary cirrhosis[J]. Lancet, 2015, 386(10003): 1565-1575. DOI: 10.1016/S0140-6736(15)00154-3
    [2]
    ADDISON TGW. On a certain affection of the skin, vitiligo idea-α plana, β tuberosa with remarks and plates[J]. Guys Hosp Rep, 1851, 7: 265-276.
    [3]
    WANG L, GERSHWIN ME, WANG FS. Primary biliary cholangitis in China[J]. Curr Opin Gastroenterol, 2016, 32(3): 195-203. http://www.ncbi.nlm.nih.gov/pubmed/26885951
    [4]
    HARMS MH, de VEER RC, LAMMERS WJ, et al. Number needed to treat with ursodeoxycholic acid therapy to prevent liver transplantation or death in primary biliary cholangitis[J]. Gut, 2020, 69(8): 1502-1509. DOI: 10.1136/gutjnl-2019-319057
    [5]
    LIERMANN GARCIA RF, EVANGELISTA GARCIA C, MCMASTER P, et al. Transplantation for primary biliary cirrhosis: Retrospective analysis of 400 patients in a single center[J]. Hepatology, 2001, 33(1): 22-27. DOI: 10.1053/jhep.2001.20894
    [6]
    BOSCH A, DUMORTIER J, MAUCORT-BOULCH D, et al. Preventive administration of UDCA after liver transplantation for primary biliary cirrhosis is associated with a lower risk of disease recurrence[J]. J Hepatol, 2015, 63(6): 1449-1458. DOI: 10.1016/j.jhep.2015.07.038
    [7]
    RONCA V, MANCUSO C, MILANI C, et al. Immune system and cholangiocytes: A puzzling affair in primary biliary cholangitis[J]. J Leukoc Biol, 2020, 108(2): 659-671. DOI: 10.1002/JLB.5MR0320-200R
    [8]
    URNO K, AIBA Y, HITOMI Y, et al. Integrated GWAS and mRNA microarray analysis identified IFNG and CD40L as the central upstream regulators in primary biliary cholangitis[J]. Hepatol Commun, 2020, 4(5): 724-738. DOI: 10.1002/hep4.1497
    [9]
    BILZER M, ROGGEL F, GERBES AL. Role of Kupffer cells in host defense and liver disease[J]. Liver Int, 2006, 26(10): 1175-1186. DOI: 10.1111/j.1478-3231.2006.01342.x
    [10]
    DAMBACH DM, WATSON LM, GRAY KR, et al. Role of CCR2 in macrophage migration into the liver during acetaminophen-induced hepatotoxicity in the mouse[J]. Hepatology, 2002, 35(5): 1093-1103. DOI: 10.1053/jhep.2002.33162
    [11]
    HAN XF. Expression level of TAM receptors signaling pathway in primary biliary cirrhosis and its regulatory mechanism in macrophage polarization[D]. Shanghai: Shanghai Jiaotong University, 2011. (in Chinese)

    韩晓凤. 巨噬细胞极化在原发性胆汁性肝硬化中的作用[D]. 上海: 上海交通大学, 2011.
    [12]
    QIN BD. Expression level of TAM receptors signaling pathway in primary biliary cirrhosis and its regulatory mechanism in macrophage polarization[D]. Shanghai: The Second Military Medical University, 2016. (in Chinese)

    秦保东. TAM信号通路在原发性胆汁性肝硬化患者中的表达水平及其对巨噬细胞极化的影响[D]. 上海: 第二军医大学, 2016.
    [13]
    FU HY, BAO WM, YANG CX, et al. Kupffer cells regulate natural killer cells via the NK group 2, Member D (NKG2D)/Retinoic Acid Early Inducible-1 (RAE-1) interaction and cytokines in a primary biliary cholangitis mouse model[J]. Med Sci Monit, 2020, 26: e923726.
    [14]
    SATO K, HALL C, GLASER S, et al. Pathogenesis of Kupffer cells in cholestatic liver injury[J]. Am J Pathol, 2016, 186(9): 2238-2247. DOI: 10.1016/j.ajpath.2016.06.003
    [15]
    OSAWA Y, SEKI E, ADACHI M, et al. Role of acid sphingomyelinase of Kupffer cells in cholestatic liver injury in mice[J]. Hepatology, 2010, 51(1): 237-245. DOI: 10.1002/hep.23262
    [16]
    TOMIYAMA T, YANG GX, ZHAO M, et al. The modulation of co-stimulatory molecules by circulating exosomes in primary biliary cirrhosis[J]. Cell Mol Immunol, 2017, 14(3): 276-284. DOI: 10.1038/cmi.2015.86
    [17]
    ALABRABA EB, LAI V, BOON L, et al. Coculture of human liver macrophages and cholangiocytes leads to CD40-dependent apoptosis and cytokine secretion[J]. Hepatology, 2008, 47(2): 552-562. http://www.ncbi.nlm.nih.gov/pubmed/17999420/
    [18]
    TEDESCO D, THAPA M, CHIN CY, et al. Alterations in intestinal microbiota lead to production of interleukin 17 by intrahepatic γδ T-cell receptor-positive cells and pathogenesis of cholestatic liver disease[J]. Gastroenterology, 2018, 154(8): 2178-2193. DOI: 10.1053/j.gastro.2018.02.019
    [19]
    LI Y, TANG R, LEUNG P, et al. Bile acids and intestinal microbiota in autoimmune cholestatic liver diseases[J]. Autoimmun Rev, 2017, 16(9): 885-896. DOI: 10.1016/j.autrev.2017.07.002
    [20]
    YANG WX, TANG YM. Role of hepatic macrophages in the development and progression of primary biliary cholangitis[J]. J Clin Hepatol, 2020, 36(4): 936-939. (in Chinese) DOI: 10.3969/j.issn.1001-5256.2020.04.051

    杨文霞, 唐映梅. 肝巨噬细胞在原发性胆汁性胆管炎发生发展中的作用[J]. 临床肝胆病杂志, 2020, 36(4): 936-939. DOI: 10.3969/j.issn.1001-5256.2020.04.051
    [21]
    WANG YQ, MAO JB, ZHOU MQ, et al. Polysaccharide from Phellinus Igniarius activates TLR4-mediated signaling pathways in macrophages and shows immune adjuvant activity in mice[J]. Int J Biol Macromol, 2019, 123: 157-166. DOI: 10.1016/j.ijbiomac.2018.11.066
    [22]
    COSOLA C, DE ANGELIS M, ROCCHETTI MT, et al. Beta-glucans supplementation associates with reduction in P-Cresyl sulfate levels and improved endothelial vascular reactivity in healthy individuals[J]. PLoS One, 2017, 12(1): e0169635. DOI: 10.1371/journal.pone.0169635
    [23]
    MA X, ZHAO YL, ZHU Y, et al. Paeonia lactiflora Pall. protects against ANIT-induced cholestasis by activating Nrf2 via PI3K/Akt signaling pathway[J]. Drug Des Devel Ther, 2015, 9: 5061-5074. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4562737/
    [24]
    PAROLA M, ROBINO G. Oxidative stress-related molecules and liver fibrosis[J]. J Hepatol, 2001, 35(2): 297-306. DOI: 10.1016/S0168-8278(01)00142-8
    [25]
    GE X, ARRIAZU E, MAGDALENO F, et al. High mobility group Box-1 drives fibrosis progression signaling via the receptor for advanced glycation end products in mice[J]. Hepatology, 2018, 68(6): 2380-2404. DOI: 10.1002/hep.30093
    [26]
    NI HM, WOOLBRIGHT BL, WILLIAMS J, et al. Nrf2 promotes the development of fibrosis and tumorigenesis in mice with defective hepatic autophagy[J]. J Hepatol, 2014, 61: 617-625. DOI: 10.1016/j.jhep.2014.04.043
    [27]
    LODDER J, DENAЁS T, CHOBERT MN, et al. Macrophage autophagy protects against liver fibrosis in mice[J]. Autophagy, 2015, 11(8): 1280-1292. DOI: 10.1080/15548627.2015.1058473
    [28]
    ALZAID F, LAGADEC F, ALBUQUERQUE M, et al. IRF5 governs liver macrophage activation that promotes hepatic fibrosis in mice and humans[J]. JCI Insight, 2016, 1(20): e88689. http://europepmc.org/articles/PMC5135279
    [29]
    ASGHAR K, BRAIN J, PALMER JM, et al. Potential role of indoleamine 2, 3-dioxygenase in primary biliary cirrhosis[J]. Oncol Lett, 2017, 14(5): 5497-5504. http://www.ingentaconnect.com/content/sp/ol/2017/00000014/00000005/art00059
    [30]
    European Association for the Study of the Liver. EASL clinical practice guidelines: The diagnosis and management of patients with primary biliary cholangitis[J]. J Hepatol, 2017, 67(1): 145-172. DOI: 10.1016/j.jhep.2017.03.022
    [31]
    JING XD, YAO JN, LI YL, et al. Risk factors for hepatocellular cancer occurrence in patients with primary biliary cholangitis[J]. Chin J Clin Oncol, 2019, 46(16): 836-840. (in Chinese) DOI: 10.3969/j.issn.1000-8179.2019.16.719

    井小笛, 姚建宁, 李艳乐, 等. 原发性胆汁性胆管炎患者发生肝癌的危险因素研究[J]. 中国肿瘤临床, 2019, 46(16): 836-840. DOI: 10.3969/j.issn.1000-8179.2019.16.719
    [32]
    LI ZM, ZHAO DT, FENG X, et al. The characteristic of auto-antibodies of hepatocellular carcinoma in primary biliary cirrhosis[J]. Chin J Lab Diag, 2014, 18(1): 59-61. (in Chinese) https://www.cnki.com.cn/Article/CJFDTOTAL-ZSZD201401019.htm

    李卓敏, 赵丹彤, 冯霞, 等. 原发性胆汁性肝硬化所致肝癌患者自身抗体特征分析[J]. 中国实验诊断学, 2014, 18(1): 59-61. https://www.cnki.com.cn/Article/CJFDTOTAL-ZSZD201401019.htm
    [33]
    WAIDMANN O, PLELI T, WEIGERT A, et al. Tax1BP1 limits hepatic inflammation and reduces experimental hepatocarcinogenesis[J]. Sci Rep, 2020, 10(1): 16264. DOI: 10.1038/s41598-020-73387-4
    [34]
    WU H, ZHONG Z, WANG A, et al. LncRNA FTX represses the progression of non-alcoholic fatty liver disease to hepatocellular carcinoma via regulating the M1/M2 polarization of Kupffer cells[J]. Cancer Cell Int, 2020, 20: 266. DOI: 10.1186/s12935-020-01354-0
    [35]
    YOU Q, CHENG L, KEDL RM, et al. Mechanism of T cell tolerance induction by murine hepatic Kupffer cells[J]. Hepatology, 2008, 48(3): 978-990. DOI: 10.1002/hep.22395
    [36]
    KUANG DM, ZHAO Q, PENG C, et al. Activated monocytes in peritumoral stroma of hepatocellular carcinoma foster immune privilege and disease progression through PD-L1[J]. J Exp Med, 2009, 206(6): 1327-1337. DOI: 10.1084/jem.20082173
    [37]
    LI H, WU K, TAO K, et al. Tim-3/galectin-9 signaling pathway mediates T-cell dysfunction and predicts poor prognosis in patients with hepatitis B virus-associated hepatocellular carcinoma[J]. Hepatology, 2012, 56(4): 1342-1351. DOI: 10.1002/hep.25777
  • 加载中

Catalog

    通讯作者: 陈斌, bchen63@163.com
    • 1. 

      沈阳化工大学材料科学与工程学院 沈阳 110142

    1. 本站搜索
    2. 百度学术搜索
    3. 万方数据库搜索
    4. CNKI搜索

    Article Metrics

    Article views (650) PDF downloads(36) Cited by()
    Proportional views
    Related

    /

    DownLoad:  Full-Size Img  PowerPoint
    Return
    Return