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

巨噬细胞在移植后慢性排斥反应中的作用研究进展

任滌非, 廖涛, 苗芸. 巨噬细胞在移植后慢性排斥反应中的作用研究进展[J]. 器官移植, 2023, 14(3): 358-363. doi: 10.3969/j.issn.1674-7445.2023.03.006
引用本文: 任滌非, 廖涛, 苗芸. 巨噬细胞在移植后慢性排斥反应中的作用研究进展[J]. 器官移植, 2023, 14(3): 358-363. doi: 10.3969/j.issn.1674-7445.2023.03.006
Ren Difei, Liao Tao, Miao Yun. Research progress on the role of macrophages in post-transplantation chronic rejection[J]. ORGAN TRANSPLANTATION, 2023, 14(3): 358-363. doi: 10.3969/j.issn.1674-7445.2023.03.006
Citation: Ren Difei, Liao Tao, Miao Yun. Research progress on the role of macrophages in post-transplantation chronic rejection[J]. ORGAN TRANSPLANTATION, 2023, 14(3): 358-363. doi: 10.3969/j.issn.1674-7445.2023.03.006

巨噬细胞在移植后慢性排斥反应中的作用研究进展

doi: 10.3969/j.issn.1674-7445.2023.03.006
基金项目: 

国家自然科学基金 82270784

国家自然科学基金 82070770

国家自然科学基金 82170767

大学生创新创业训练计划项目 202212121242

详细信息
    作者简介:
    通讯作者:

    苗芸(ORCID:0000-0003-3592-4695),博士,主任医师,研究方向为肾移植,Email:miaoyunecho@126.com

  • 中图分类号: R617, R329.2

Research progress on the role of macrophages in post-transplantation chronic rejection

More Information
  • 摘要: 器官移植是治疗终末期器官病变的最佳方法,然而排斥反应仍然是影响移植物存活的重要因素。目前,针对急性排斥反应的治疗方法效果良好,但对慢性排斥反应仍缺乏有效的治疗手段,长期慢性排斥反应可能导致移植物失功,严重影响移植物的长期存活率。近年来,巨噬细胞在慢性排斥反应中的作用逐渐受到关注。本文对慢性排斥反应的主要病理变化、参与慢性排斥反应巨噬细胞的多样性及功能差异、巨噬细胞参与慢性排斥反应的作用及机制进行综述,并总结巨噬细胞相关慢性排斥反应治疗的研究进展,以期为巨噬细胞在器官移植术后慢性排斥反应中的作用研究提供参考。

     

  • [1] VASCO M, BENINCASA G, FIORITO C, et al. Clinical epigenetics and acute/chronic rejection in solid organ transplantation: an update[J]. Transplant Rev (Orlando), 2021, 35(2): 100609. DOI: 10.1016/j.trre.2021.100609.
    [2] ZHANG H, LI Z, LI W. M2 macrophages serve as critical executor of innate immunity in chronic allograft rejection[J]. Front Immunol, 2021, 12: 648539. DOI: 10.3389/fimmu.2021.648539.
    [3] CHEN S, LAKKIS FG, LI XC. The many shades of macrophages in regulating transplant outcome[J]. Cell Immunol, 2020, 349: 104064. DOI: 10.1016/j.cellimm.2020.104064.
    [4] GOSWAMI R. The current state of artificial intelligence in cardiac transplantation[J]. Curr Opin Organ Transplant, 2021, 26(3): 296-301. DOI: 10.1097/MOT.0000000000000875.
    [5] LAI X, ZHENG X, MATHEW JM, et al. Tackling chronic kidney transplant rejection: challenges and promises[J]. Front Immunol, 2021, 12: 661643. DOI: 10.3389/fimmu.2021.661643.
    [6] ANGELICO R, SENSI B, MANZIA TM, et sl. Chronic rejection after liver transplantation: opening the Pandora's box[J]. World J Gastroenterol, 2021, 27(45): 7771-7783. DOI: 10.3748/wjg.v27.i45.7771.
    [7] FRANZ M, NERI D, BERNDT A. Chronic cardiac allograft rejection: critical role of ED-A(+) fibronectin and implications for targeted therapy strategies[J]. J Pathol, 2012, 226(4): 557-561. DOI: 10.1002/path.3968.
    [8] LI T, ZHANG Z, BARTOLACCI JG, et al. Graft IL-33 regulates infiltrating macrophages to protect against chronic rejection[J]. J Clin Invest, 2020, 130(10): 5397-5412. DOI: 10.1172/JCI133008.
    [9] LUO Y, SHAO L, CHANG J, et al. M1 and M2 macrophages differentially regulate hematopoietic stem cell self-renewal and ex vivo expansion[J]. Blood Adv, 2018, 2(8): 859-870. DOI: 10.1182/bloodadvances.2018015685.
    [10] NAKAI K. Multiple roles of macrophage in skin[J]. J Dermatol Sci, 2021, 104(1): 2-10. DOI: 10.1016/j.jdermsci.2021.08.008.
    [11] FLEMING BD, CHANDRASEKARAN P, DILLON LA, et al. The generation of macrophages with anti-inflammatory activity in the absence of STAT6 signaling[J]. J Leukoc Biol, 2015, 98(3): 395-407. DOI: 10.1189/jlb.2A1114-560R.
    [12] ZHANG F, ZHANG J, CAO P, et al. The characteristics of regulatory macrophages and their roles in transplantation[J]. Int Immunopharmacol, 2021, 91: 107322. DOI: 10.1016/j.intimp.2020.107322.
    [13] HOU Y, ZHU L, TIAN H, et al. IL-23-induced macrophage polarization and its pathological roles in mice with imiquimod-induced psoriasis[J]. Protein Cell, 2018, 9(12): 1027-1038. DOI: 10.1007/s13238-018-0505-z.
    [14] ARABPOUR M, SAGHAZADEH A, REZAEI N. Anti-inflammatory and M2 macrophage polarization-promoting effect of mesenchymal stem cell-derived exosomes[J]. Int Immunopharmacol, 2021, 97: 107823. DOI: 10.1016/j.intimp.2021.107823.
    [15] MU X, LI Y, FAN GC. Tissue-resident macrophages in the control of infection and resolution of inflammation[J]. Shock, 2021, 55(1): 14-23. DOI: 10.1097/SHK.0000000000001601.
    [16] ESCHLUNDT C, FISCHER H, BUCHER CH, et al. The multifaceted roles of macrophages in bone regeneration: a story of polarization, activation and time[J]. Acta Biomater, 2021, 133: 46-57. DOI: 10.1016/j.actbio.2021.04.052.
    [17] HIRAO H, NAKAMURA K, KUPIEC-WEGLINSKI JW. Liver ischaemia-reperfusion injury: a new understanding of the role of innate immunity[J]. Nat Rev Gastroenterol Hepatol, 2022, 19(4): 239-256. DOI: 10.1038/s41575-021-00549-8.
    [18] ELCHANINOV A, VISHNYAKOVA P, MENYAILO E, et al. An eye on kupffer cells: development, phenotype and the macrophage niche[J]. Int J Mol Sci, 2022, 23(17): 9868. DOI: 10.3390/ijms23179868.
    [19] TRAN S, BABA I, POUPEL L, et al. Impaired kupffer cell self-renewal alters the liver response to lipid overload during non-alcoholic steatohepatitis[J]. Immunity, 2020, 53(3): 627-640. DOI: 10.1016/j.immuni.2020.06.003.
    [20] SHEN Q, WANG Y, CHEN J, et al. Single-cell RNA sequencing reveals the immunological profiles of renal allograft rejection in mice[J]. Front Immunol, 2021, 12: 693608. DOI: 10.3389/fimmu.2021.693608.
    [21] SABLIK KA, JORDANOVA ES, POCORNI N, et al. Immune cell infiltrate in chronic-active antibody-mediated rejection[J]. Front Immunol, 2020, 10: 3106. DOI: 10.3389/fimmu.2019.03106.
    [22] VAN DEN BOSCH TPP, HILBRANDS LB, KRAAIJEVELD R, et al. Pretransplant numbers of CD16+ monocytes as a novel biomarker to predict acute rejection after kidney transplantation: a pilot study[J]. Am J Transplant, 2017, 17(10): 2659-2667. DOI: 10.1111/ajt.14280.
    [23] KAUL AM, GOPARAJU S, DVORINA N, et al. Acute and chronic rejection: compartmentalization and kinetics of counterbalancing signals in cardiac transplants[J]. Am J Transplant, 2015, 15(2): 333-345. DOI: 10.1111/ajt.13014.
    [24] WU C, ZHAO Y, XIAO X, et al. Graft-infiltrating macrophages adopt an M2 phenotype and are inhibited by purinergic receptor P2X7 antagonist in chronic rejection[J]. Am J Transplant, 2016, 16(9): 2563-2573. DOI: 10.1111/ajt.13808.
    [25] KITCHENS WH, CHASE CM, UEHARA S, et al. Macrophage depletion suppresses cardiac allograft vasculopathy in mice[J]. Am J Transplant, 2007, 7(12): 2675-2682. DOI: 10.1111/j.1600-6143.2007.01997.x.
    [26] MITCHELL RN. Graft vascular disease: immune response meets the vessel wall[J]. Annu Rev Pathol, 2009, 4: 19-47. DOI: 10.1146/annurev.pathol.3.121806.151449.
    [27] FILIĆ V, MIJANOVIĆ L, PUTAR D, et al. Regulation of the actin cytoskeleton via Rho GTPase signalling in dictyostelium and mammalian cells: a parallel slalom[J]. Cells, 2021, 10(7): 1592. DOI: 10.3390/cells10071592.
    [28] KLOC M, UOSEF A, VILLAGRAN M, et al. RhoA- and actin-dependent functions of macrophages from the rodent cardiac transplantation model perspective -timing is the essence[J]. Biology (Basel), 2021, 10(2): 70. DOI: 10.3390/biology10020070.
    [29] LIU Y, CHEN W, MINZE LJ, et al. Dissonant response of M0/M2 and M1 bone-marrow-derived macrophages to RhoA pathway interference[J]. Cell Tissue Res, 2016, 366(3): 707-720. DOI: 10.1007/s00441-016-2491-x.
    [30] VERHEIJ M, ZEERLEDER S, VOERMANS C. Heme oxygenase-1: equally important in allogeneic hematopoietic stem cell transplantation and organ transplantation?[J]. Transpl Immunol, 2021, 68: 101419. DOI: 10.1016/j.trim.2021.101419.
    [31] TOKI D, ZHANG W, HOR KL, et al. The role of macrophages in the development of human renal allograft fibrosis in the first year after transplantation[J]. Am J Transplant, 2014, 14(9): 2126-2136. DOI: 10.1111/ajt.12803.
    [32] WANG X, CHEN J, XU J, et al. The role of macrophages in kidney fibrosis[J]. Front Physiol, 2021, 12: 705838. DOI: 10.3389/fphys.2021.705838.
    [33] WANG YY, JIANG H, PAN J, et al. Macrophage-to-myofibroblast transition contributes to interstitial fibrosis in chronic renal allograft injury[J]. J Am Soc Nephrol, 2017, 28(7): 2053-2067. DOI: 10.1681/ASN.2016050573.
    [34] ZOU H, MING B, LI J, et al. Extracellular HMGB1 contributes to the chronic cardiac allograft vasculopathy/fibrosis by modulating TGF-β1 signaling[J]. Front Immunol, 2021, 12: 641973. DOI: 10.3389/fimmu.2021.641973.
    [35] SCHAUERTE C, HÜBNER A, RONG S, et al. Antagonism of profibrotic microRNA-21 improves outcome of murine chronic renal allograft dysfunction[J]. Kidney Int, 2017, 92(3): 646-656. DOI: 10.1016/j.kint.2017.02.012.
    [36] BALAM S, BUCHTLER S, WINTER F, et al. Donor-but not recipient-derived cells produce collagen-1 in chronically rejected cardiac allografts[J]. Front Immunol, 2022, 12: 816509. DOI: 10.3389/fimmu.2021.816509.
    [37] 王光川, LI XC. 天然免疫细胞的获得性免疫属性及其在移植排斥中的作用[J]. 中华消化外科杂志, 2022, 21(8): 1044-1049. DOI: 10.3760/cma.j.cn115610-20220628-00376.

    WANG GC, LI XC. Features of acquired immune properties in innate immune cells and its roles in transplant rejection[J]. Chin J Dig Surg, 2022, 21(8): 1044-1049. DOI: 10.3760/cma.j.cn115610-20220628-00376.
    [38] 罗登科. 巨噬细胞在器官移植免疫排斥反应中的研究进展[J]. 海南医学, 2022, 33(16): 2148-2152. DOI: 10.3969/j.issn.1003-6350.2022.16.029.

    LUO DK. Research progress of macrophages in immune rejection of organ transplantation[J]. Hainan Med J, 2022, 33(16): 2148-2152. DOI: 10.3969/j.issn.1003-6350.2022.16.029.
    [39] SUBUDDHI A, UOSEF A, ZOU D, et al. Comparative transcriptome profile of mouse macrophages treated with the RhoA/Rock pathway inhibitors Y27632, Fingolimod (Gilenya), and Rezurock (Belumosudil, SLx-2119)[J]. Int Immunopharmacol, 2023, 118: 110017. DOI: 10.1016/j.intimp.2023.110017.
    [40] CHEN W, CHEN W, CHEN S, et al. Fingolimod (FTY720) prevents chronic rejection of rodent cardiac allografts through inhibition of the RhoA pathway[J]. Transpl Immunol, 2021, 65: 101347. DOI: 10.1016/j.trim.2020.101347.
    [41] LIU Y, CHEN W, WU C, et al. Macrophage/monocyte-specific deletion of Ras homolog gene family member A (RhoA) downregulates fractalkine receptor and inhibits chronic rejection of mouse cardiac allografts[J]. J Heart Lung Transplant, 2017, 36(3): 340-354. DOI: 10.1016/j.healun.2016.08.011.
    [42] UOSEF A, VAUGHN N, CHU X, et al. Siponimod (Mayzent) downregulates RhoA and cell surface expression of the S1P1 and CX3CR1 receptors in mouse RAW 264.7 macrophages[J]. Arch Immunol Ther Exp (Warsz), 2020, 68(3): 19. DOI: 10.1007/s00005-020-00584-4.
    [43] USUELLI V, BEN NASR M, D'ADDIO F, et al. miR-21 antagonism reprograms macrophage metabolism and abrogates chronic allograft vasculopathy[J]. Am J Transplant, 2021, 21(10): 3280-3295. DOI: 10.1111/ajt.16581.
    [44] ZHANG Z, ZHANG N, SHI J, et al. Allograft or recipient ST2 deficiency oppositely affected cardiac allograft vasculopathy via differentially altering immune cells infiltration[J]. Front Immunol, 2021, 12: 657803. DOI: 10.3389/fimmu.2021.657803.
  • 加载中
图(1)
计量
  • 文章访问数:  232
  • HTML全文浏览量:  93
  • PDF下载量:  68
  • 被引次数: 0
出版历程
  • 收稿日期:  2022-12-04
  • 刊出日期:  2023-05-15

目录

    /

    返回文章
    返回