切换至 "中华医学电子期刊资源库"

中华细胞与干细胞杂志(电子版) ›› 2024, Vol. 14 ›› Issue (01) : 45 -50. doi: 10.3877/cma.j.issn.2095-1221.2024.01.007

综述

免疫细胞在肾脏缺血再灌注损伤修复中的作用研究进展
曹守青1, 来东2, 焦启龙3, 安哲昆4, 李修彬2,()   
  1. 1. 075000 张家口,河北北方学院研究生院;100039 北京,解放军总医院第三医学中心泌尿外科医学部
    2. 100039 北京,解放军总医院第三医学中心泌尿外科医学部
    3. 100039 北京,解放军总医院第三医学中心泌尿外科医学部;300071 天津,南开大学医学院
    4. 030001 太原,山西医科大学基础医学院
  • 收稿日期:2023-10-24 出版日期:2024-02-01
  • 通信作者: 李修彬
  • 基金资助:
    国家自然科学基金青年科学基金(81802804); 军队医学科技青年培育计划孵化项目(19QNP060); 解放军总医院"优青"培育专项(2020-YQPY-006); 解放军总医院青年自主创新科学基金成长项目(22QNCZ029)

The role of immune cells in renal ischemia-reperfusion injury and repair

Shouqing Cao1, Dong Lai2, Qilong Jiao3, Zhekun An4, Xiubin Li2,()   

  1. 1. College of Graduate, Hebei North University, Zhangjiakou 075000, China; Department of Urology, the Third Medical Center, Chinese PLA General Hospital, Beijing 100039, China
    2. Department of Urology, the Third Medical Center, Chinese PLA General Hospital, Beijing 100039, China
    3. Department of Urology, the Third Medical Center, Chinese PLA General Hospital, Beijing 100039, China; Medical School of Nankai University, Tianjin 300071, China
    4. School of Basic Medicine, Shanxi Medical University, Taiyuan 030001, China
  • Received:2023-10-24 Published:2024-02-01
  • Corresponding author: Xiubin Li
引用本文:

曹守青, 来东, 焦启龙, 安哲昆, 李修彬. 免疫细胞在肾脏缺血再灌注损伤修复中的作用研究进展[J/OL]. 中华细胞与干细胞杂志(电子版), 2024, 14(01): 45-50.

Shouqing Cao, Dong Lai, Qilong Jiao, Zhekun An, Xiubin Li. The role of immune cells in renal ischemia-reperfusion injury and repair[J/OL]. Chinese Journal of Cell and Stem Cell(Electronic Edition), 2024, 14(01): 45-50.

急性肾损伤(AKI)是一种常见的临床综合征,我国住院人群AKI的发病率高达11.6%,AKI发生后容易进展为慢性肾病(CKD)甚至终末期肾病(ESRD)。缺血再灌注损伤(IRI)是AKI的主要病因之一。肾小管上皮细胞是IRI致AKI发生过程中受损的主要细胞类型,也是肾脏修复过程中细胞再生的主要细胞来源。在AKI发生发展以及损伤修复的过程中,免疫细胞能够调节肾小管上皮细胞的损伤、增殖以及再上皮化等多种生物过程,最终导致AKI的不同结局。本文就IRI导致的AKI发生过程中免疫细胞发挥的作用以及领域内的挑战和发展作一综述。

Acute kidney injury (AKI) is a common clinical syndrome. The total incidence of AKI in hospitalized population in China is as high as 11.6%, and the occurrence of AKI is easy to progress to chronic kidney disease (CKD) and even end-stage renal disease (ESRD) . Ischemia-reperfusion injury (IRI) is one of the major causes of AKI. Renal tubular epithelial cells are the main cell types damaged in the process of IRI induced AKI, and also the main cell source of cell regeneration in the process of kidney repair. During the development and repair of AKI, immune cells regulate the damage, proliferation and re-epithelialization of renal tubular epithelial cells and other biological processes, which eventually lead to different outcomes of AKI. In this paper, the role of immune cells in the process of AKI induced by IRI and the challenges and developments in the field are reviewed.

1
Lewington AJ, Cerda J, Mehta RL. Raising awareness of acute kidney injury: a global perspective of a silent killer[J]. Kidney Int, 2013, 84(3):457-467.
2
Xu X, Nie S, Liu Z, et al. Epidemiology and clinical correlates of AKI in Chinese hospitalized adults[J]. Clin J Am Soc Nephrol, 2015, 10(9):1510-1518.
3
Chawla LS, Eggers PW, Star RA, et al. Acute kidney injury and chronic kidney disease as interconnected syndromes[J]. N Engl J Med, 2014, 371(1):58-66.
4
Kinsey GR, Li L, Okusa MD. Inflammation in acute kidney injury[J]. Nephron Exp Nephrol, 2008, 109(4):e102-107.
5
Jang HR, Rabb H. The innate immzzune response in ischemic acute kidney injury[J]. Clin Immunol, 2009, 130(1):41-50.
6
Venkatachalam MA, Weinberg JM, Kriz W, et al. Failed tubule recovery, AKI-CKD transition, and kidney disease progression[J]. J Am Soc Nephrol, 2015, 26(8):1765-1776.
7
Sharfuddin AA, Molitoris BA. Pathophysiology of ischemic acute kidney injury[J]. Nat Rev Nephrol, 2011, 7(4):189-200.
8
Melo Ferreira R, Sabo AR, Winfree S, et al. Integration of spatial and single-cell transcriptomics localizes epithelial cell-immune cross-talk in kidney injury[J]. JCI Insight, 2021, 6(12):e147703. doi: 10.1172/jci.insight.147703.
9
Rudman-Melnick V, Adam M, Potter A, et al. Single-cell profiling of AKI in a murine model reveals novel transcriptional signatures, profibrotic phenotype, and epithelial-to-stromal crosstalk[J]. J Am Soc Nephrol, 2020, 31(12):2793-2814.
10
Kirita Y, Wu H, Uchimura K, et al. Cell profiling of mouse acute kidney injury reveals conserved cellular responses to injury[J]. Proc Natl Acad Sci U S A, 2020, 117(27):15874-15883.
11
Wu H, Kirita Y, Donnelly EL, et al. Advantages of single-nucleus over single-cell RNA sequencing of adult kidney: rare cell types and novel cell states revealed in fibrosis[J]. J Am Soc Nephrol, 2019, 30(1):23-32.
12
Devarajan P. Update on mechanisms of ischemic acute kidney injury[J]. J Am Soc Nephrol, 2006, 17(6):1503-1520.
13
Awad AS, Rouse M, Huang L, et al. Compartmentalization of neutrophils in the kidney and lung following acute ischemic kidney injury[J]. Kidney Int, 2009, 75(7):689-698.
14
Cho W, Song J, Oh S, et al. Fate of neutrophils during the recovery phase of ischemia/reperfusion induced acute kidney injury[J]. J Korean Med Sci, 2017, 32(10):1616-1625.
15
Li L, Huang L, Vergis AL, et al. IL-17 produced by neutrophils regulates IFN-gamma-mediated neutrophil migration in mouse kidney ischemia-reperfusion injury[J]. J Clin Invest, 2010, 120(1):331-342.
16
Li H, Han SJ, Kim M, et al. Divergent roles for kidney proximal tubule and granulocyte PAD4 in ischemic AKI[J]. Am J Physiol Renal Physiol, 2018, 314(5):F809-F819.
17
Thomas K, Zondler L, Ludwig N, et al. Glutamine prevents acute kidney injury by modulating oxidative stress and apoptosis in tubular epithelial cells[J]. JCI Insight, 2022, 7(21):e163161. doi: 10.1172/jci.insight.163161.
18
Wu X, You D, Pan M, et al. Knockout of the C3a receptor protects against renal ischemia reperfusion injury by reduction of NETs formation[J]. Cell Mol Life Sci, 2023, 80(11):322. doi: 10.1007/s00018-023-04967-6.
19
Qin L, Li G, Kirkiles-Smith N, et al. Complement C5 inhibition reduces T cell-mediated allograft vasculopathy caused by both alloantibody and ischemia reperfusion injury in humanized mice[J]. Am J Transplant, 2016, 16(10):2865-2876.
20
Yao W, Chen Y, Li Z, et al. Single cell RNA sequencing identifies a unique inflammatory macrophage subset as a druggable target for alleviating acute kidney injury[J]. Adv Sci (Weinh), 2022, 9(12):e2103675. doi: 10.1002/advs.202103675.
21
Han HI, Skvarca LB, Espiritu EB, et al. The role of macrophages during acute kidney injury: destruction and repair[J]. Pediatr Nephrol, 2019, 34(4):561-569.
22
Arai S, Kitada K, Yamazaki T, et al. Apoptosis inhibitor of macrophage protein enhances intraluminal debris clearance and ameliorates acute kidney injury in mice[J]. Nat Med, 2016, 22(2):183-193.
23
Allison SJ. Acute kidney injury: AIMing to enhance debris clearance and improve outcomes in AKI[J]. Nat Rev Nephrol, 2016, 12(3):123. doi: 10.1038/nrneph.2016.3.
24
Mori K, Lee HT, Rapoport D, et al. Endocytic delivery of lipocalin-siderophore-iron complex rescues the kidney from ischemia-reperfusion injury[J]. J Clin Invest, 2005, 115(3):610-621.
25
Jung M, Brune B, Hotter G, et al. Macrophage-derived Lipocalin-2 contributes to ischemic resistance mechanisms by protecting from renal injury[J]. Sci Rep, 2016, 6:21950.doi: 10.1038/srep21950.
26
Li L, Gan H, Jin H, et al. Astragaloside IV promotes microglia/macrophages M2 polarization and enhances neurogenesis and angiogenesis through PPARγ pathway after cerebral ischemia/reperfusion injury in rats[J]. Int Immunopharmacol, 2021, 92:107335.doi: 10.1016/j.intimp.2020.107335.
27
Bohlson SS, O'Conner SD, Hulsebus HJ, et al. Complement, c1q, and c1q-related molecules regulate macrophage polarization[J]. Front Immunol, 2014, 5:402. doi: 10.3389/fimmu.2014.00402.
28
Shapouri-Moghaddam A, Mohammadian S, Vazini H, et al. Macrophage plasticity, polarization, and function in health and disease[J]. J Cell Physiol, 2018, 233(9):6425-6440.
29
Ferenbach DA, Sheldrake TA, Dhaliwal K, et al. Macrophage/monocyte depletion by clodronate, but not diphtheria toxin, improves renal ischemia/reperfusion injury in mice[J]. Kidney Int, 2012, 82(8): 928-933.
30
Day YJ, Huang L, Ye H, et al. Renal ischemia-reperfusion injury and adenosine 2A receptor-mediated tissue protection: role of macrophages[J]. Am J Physiol Renal Physiol, 2005, 288(4):F722-731
31
Lech M, Grobmayr R, Ryu M, et al. Macrophage phenotype controls long-term AKI outcomes--kidney regeneration versus atrophy[J]. J Am Soc Nephrol, 2014, 25(2):292-304.
32
Linkermann A, Brasen JH, Himmerkus N, et al. Rip1 (receptor-interacting protein kinase 1) mediates necroptosis and contributes to renal ischemia/reperfusion injury[J]. Kidney Int, 2012, 81(8):751-761.
33
Xu L, Xing Z, Yuan J, et al. Ultrasmall nanoparticles regulate immune microenvironment by activating IL-33/ST2 to alleviate renal ischemia-reperfusion injury[J]. Adv Healthc Mater, 2024:e2303276. doi: 10.1002/adhm.202303276.
34
Xu L, Guo J, Moledina DG, et al. Immune-mediated tubule atrophy promotes acute kidney injury to chronic kidney disease transition[J]. Nat Commun, 2022, 13(1):4892. doi: 10.1038/s41467-022-32634-0.
35
Huang W, Wang BO, Hou YF, et al. JAML promotes acute kidney injury mainly through a macrophage-dependent mechanism[J]. JCI Insight, 2022, 7(14):e158571. doi: 10.1172/jci.insight.158571.
36
Jang HR, Gandolfo MT, Ko GJ, et al. B cells limit repair after ischemic acute kidney injury[J]. J Am Soc Nephrol, 2010, 21(4):654-665.
37
Linfert D, Chowdhry T, Rabb H. Lymphocytes and ischemia-reperfusion injury[J]. Transplant Rev (Orlando), 2009, 23(1):1-10.
38
Cao Q, Wang Y, Niu Z, et al. Potentiating tissue-resident type 2 innate lymphoid cells by IL-33 to prevent renal ischemia-reperfusion injury[J]. J Am Soc Nephrol, 2018, 29(3):961-976.
39
Mockel T, Basta F, Weinmann-Menke J, et al. B cell activating factor (BAFF): Structure, functions, autoimmunity and clinical implications in systemic lupus erythematosus (SLE)[J]. Autoimmun Rev, 2021, 20(2):102736. doi: 10.1016/j.autrev.2020.102736.
40
Tsivilika M, Doumaki E, Stavrou G, et al. The adaptive immune response in cardiac arrest resuscitation induced ischemia reperfusion renal injury[J]. 2020, 27:15. doi: 10.1186/s40709-020-00125-2.
41
Calabrese DR, Aminian E, Mallavia B, et al. Natural killer cells activated through NKG2D mediate lung ischemia-reperfusion injury[J]. 2021, 131(3):e137047.doi: 10.1172/JCI137047.
42
Lee K, Jang HR. Role of T cells in ischemic acute kidney injury and repair[J]. Korean J Intern Med, 2022, 37(3):534-550.
43
Baudoux T, Husson C, De Prez E, et al. CD4 and CD8 T cells exert regulatory properties during experimental acute aristolochic acid nephropathy[J]. 2018, 8(1):5334.
44
Ko GJ, Linfert D, Jang HR, et al. Transcriptional analysis of infiltrating T cells in kidney ischemia-reperfusion injury reveals a pathophysiological role for CCR5[J]. Am J Physiol Renal Physiol, 2012, 302(6):F762-773.
45
Pease JJEoodd. Designing small molecule CXCR3 antagonists[J]. Expert Opin Drug Discov, 2017, 12(2):159-168.
46
Marques VP, Goncalves GM, Feitoza CQ, et al. Influence of TH1/TH2 switched immune response on renal ischemia-reperfusion injury[J]. Nephron Exp Nephrol, 2006, 104(1):e48-56.
47
Guo L, Lee HH, Noriega ML, et al. Lymphocyte-specific deletion of IKK2 or NEMO mediates an increase in intrarenal Th17 cells and accelerates renal damage in an ischemia-reperfusion injury mouse model[J]. Am J Physiol Renal Physiol, 2016, 311(5):F1005-1014.
48
Turner JE, Paust HJ, Steinmetz OM, et al. The Th17 immune response in renal inflammation[J]. Kidney Int, 2010, 77(12):1070-1075.
49
Liang SC, Tan XY, Luxenberg DP, et al. Interleukin (IL)-22 and IL-17 are coexpressed by Th17 cells and cooperatively enhance expression of antimicrobial peptides[J]. J Exp Med, 2006, 203(10):2271-2279.
50
Noel S, Lee K, Gharaie S, et al. Immune checkpoint molecule TIGIT regulates kidney T cell functions and contributes to AKI[J]. J Am Soc Nephrol, 2023, 34(5):755-771.
51
Xian W, Wu J, Li Q, et al. CXCR3 alleviates renal ischemiareperfusion injury via increase of Tregs[J]. Mol Med Rep, 2021, 24(1):541. doi: 10.3892/mmr.2021.12180.
52
Jun C, Ke W, Qingshu L, et al. Protective effect of CD4(+)CD25(high)CD127(low) regulatory T cells in renal ischemia-reperfusion injury[J]. Cell Immunol, 2014, 289(1-2):106-111.
53
Jun C, Qingshu L, Ke W, et al. Protective effect of CXCR3(+)CD4(+)CD25(+)Foxp3(+) regulatory T cells in renal ischemia-reperfusion injury[J]. Mediators Inflamm, 2015, 2015:360973. doi: 10.1155/2015/360973.
54
Carbone F, De Rosa V, Carrieri PB, et al. Regulatory T cell proliferative potential is impaired in human autoimmune disease[J]. Nat Med, 2014, 20(1):69-74.
55
Boothby I, Cohen J, Rosenblum MJSi. Regulatory T cells in skin injury: At the crossroads of tolerance and tissue repair[J]. Sci Immunol, 2020, 5(47):eaaz9631. doi: 10.1126/sciimmunol.aaz9631.
56
Xu J, Li X, Yuan Q, et al. The semaphorin 4A-neuropilin 1 axis alleviates kidney ischemia reperfusion injury by promoting the stability and function of regulatory T cells[J]. Kidney Int, 2021, 100(6):1268-1281.
57
Hu C, Zhang C, Yang C. The Role of natural killer T cells in acute kidney injury: angel or evil?[J]. Curr Protein Pept Sci, 2017, 18(12):1200-1204.
58
Aoyama S, Nakagawa R, Nemoto S, et al. Checkpoint blockade accelerates a novel switch from an NKT-driven TNFα response toward a T cell driven IFN-γ response within the tumor microenvironment[J]. J Immunother Cancer, 2021, 9(6):e002269. doi: 10.1136/jitc-2020-002269.
59
Yang SH, Lee JP, Jang HR, et al. Sulfatide-reactive natural killer T cells abrogate ischemia-reperfusion injury[J]. J Am Soc Nephrol, 2011, 22(7):1305-1314.
60
Baban B, Khodadadi H, Vaibhav K, et al. Regulation of innate lymphoid cells in acute kidney injury: crosstalk between cannabidiol and GILZ[J]. J Immunol Res, 2020, 2020:6056373.doi: 10.1155/2020/6056373.
61
Deng B, Lin Y, Chen Y, et al. Plasmacytoid dendritic cells promote acute kidney injury by producing interferon-alpha[J]. Cell Mol Immunol, 2021, 18(1):219-229.
62
Salei N, Rambichler S, Salvermoser J, et al. The kidney contains ontogenetically distinct dendritic cell and macrophage subtypes throughout development that differ in their inflammatory properties[J]. J Am Soc Nephrol, 2020, 31(2):257-278.
63
Li L, Okusa MD. Macrophages, dendritic cells, and kidney ischemia-reperfusion injury[J]. Semin Nephrol, 2010, 30(3):268-277.
64
Kim MG, Boo CS, Ko YS, et al. Depletion of kidney CD11c+ F4/80+ cells impairs the recovery process in ischaemia/reperfusion-induced acute kidney injury[J]. Nephrol Dial Transplant, 2010, 25(9):2908-2921.
65
Romagnani P, Anders HJ. What can tubular progenitor cultures teach us about kidney regeneration?[J]. Kidney Int, 2013, 83(3):351-353.
66
Bajwa A, Huang L, Ye H, et al. Dendritic cell sphingosine 1-phosphate receptor-3 regulates Th1-Th2 polarity in kidney ischemia-reperfusion injury[J]. J Immunol, 2012, 189(5):2584-2596.
67
Qu J, Li D, Jin J, et al. Hypoxia-inducible factor 2α attenuates renal ischemia-reperfusion injury by suppressing CD36-mediated lipid accumulation in dendritic cells in a mouse model[J]. J Am Soc Nephrol, 2023, 34(1):73-87.
68
Saitoh SI, Abe F, Kanno A, et al. TLR7 mediated viral recognition results in focal type I interferon secretion by dendritic cells[J]. Nat Commun, 2017, 8(1):1592.
69
Deng B, Lin Y, Chen Y, et al. Plasmacytoid dendritic cells promote acute kidney injury by producing interferon-α[J]. Cell Mol Immunol, 2021, 18(1):219-229.
70
McClatchey AI, Yap AS. Contact inhibition (of proliferation) redux[J]. Curr Opin Cell Biol, 2012, 24(5):685-694.
71
Liu J, Kumar S, Dolzhenko E, et al. Molecular characterization of the transition from acute to chronic kidney injury following ischemia/reperfusion[J]. JCI Insight, 2017, 2(18):e94716. doi:10.1172/jci.insight.94716.
72
Zhang D, Xing Y, Li W, et al. Renal tubules transcriptome reveals metabolic maladaption during the progression of ischemia-induced acute kidney injury[J]. Biochem Biophys Res Commun, 2018, 505(2):432-438.
73
Battistone MA, Mendelsohn AC, Spallanzani RG, et al. Proinflammatory P2Y14 receptor inhibition protects against ischemic acute kidney injury in mice[J]. J Clin Invest, 2020, 130(7):3734-3749.
74
Liang Y, Sun X, Wang M, et al. PP2Acα promotes macrophage accumulation and activation to exacerbate tubular cell death and kidney fibrosis through activating Rap1 and TNFα production[J]. Cell Death Differ, 2021, 28(9):2728-2744.
75
Baek JH, Zeng R, Weinmann-Menke J, et al. IL-34 mediates acute kidney injury and worsens subsequent chronic kidney disease[J]. J Clin Invest, 2015, 125(8):3198-3214.
[1] 刘欢, 邢皓, 常正奇, 张记. 机械敏感性离子通道蛋白Piezo1在感染相关疾病中的研究进展[J/OL]. 中华实验和临床感染病杂志(电子版), 2024, 18(05): 263-269.
[2] 钱龙, 陆晓峰, 王行舟, 杜峻峰, 沈晓菲, 管文贤. 神经系统调控胃肠道肿瘤免疫应答研究进展[J/OL]. 中华普外科手术学杂志(电子版), 2024, 18(01): 86-89.
[3] 中国医疗保健国际交流促进会肝脏移植学分会, 中国医疗保健国际交流促进会肾脏移植学分会, 中国医药生物技术协会生物诊断技术分会. 免疫细胞功能状态量化检测评估与临床应用专家共识[J/OL]. 中华移植杂志(电子版), 2024, 18(02): 65-73.
[4] 曹飞, 庞俊. 前列腺癌免疫微环境中免疫抑制性细胞分类及其作用机制[J/OL]. 中华腔镜泌尿外科杂志(电子版), 2024, 18(02): 121-125.
[5] 王大伟, 陆雅斐, 皇甫少华, 陈玉婷, 陈澳, 江滨. 间充质干细胞通过调控免疫机制促进创面愈合的研究进展[J/OL]. 中华细胞与干细胞杂志(电子版), 2024, 14(06): 361-366.
[6] 梅杰, 徐瑞, 蔡芸, 朱一超. 纤维化对肿瘤浸润免疫细胞的影响——“硬冷肿瘤”的形成[J/OL]. 中华细胞与干细胞杂志(电子版), 2024, 14(05): 257-263.
[7] 朱兴墅, 郑师尧, 王庆惠, 陈力, 刘旺武, 纪辉涛, 王瑜, 赵虎, 方永超. 蛋白磷酸酶-1催化亚基β在结直肠癌诊断、预后及免疫浸润中的生物信息学分析[J/OL]. 中华细胞与干细胞杂志(电子版), 2023, 13(06): 321-330.
[8] 张杰, 田广磊, 陈雄. 基于生物信息学分析探讨肝癌BRD4与预后关系及其ceRNA调控网络构建[J/OL]. 中华肝脏外科手术学电子杂志, 2024, 13(04): 568-576.
[9] 林玲, 李京儒, 沈瑞华, 林惠, 乔晞. 基于生物信息学分析小鼠急性肾损伤和急性肺损伤的枢纽基因[J/OL]. 中华肾病研究电子杂志, 2024, 13(03): 134-144.
[10] 吴琼, 朱国贞. 膜性肾病中M2巨噬细胞相关基因的生物信息学分析[J/OL]. 中华肾病研究电子杂志, 2023, 12(03): 156-162.
[11] 杨永红, 杨莹, 齐红蕾, 刘福瑞, 朱金源. 单细胞测序在急性呼吸窘迫综合征中的应用进展[J/OL]. 中华重症医学电子杂志, 2024, 10(03): 248-252.
[12] 吴宗盛, 谢剑锋, 邱海波. 冷诱导RNA结合蛋白与炎症反应的研究进展[J/OL]. 中华重症医学电子杂志, 2024, 10(01): 42-47.
[13] 任香凝, 郑晓明. 缺血性脑卒中与外周免疫应答的研究进展[J/OL]. 中华脑科疾病与康复杂志(电子版), 2023, 13(03): 175-179.
[14] 杨麦青, 张云香. 胃癌化疗后浆膜腔大B细胞淋巴瘤一例报道并文献复习[J/OL]. 中华诊断学电子杂志, 2024, 12(03): 183-187.
[15] 孙冠超, 万军, 石卉. IgG相关食物不耐受与肠道免疫微环境相关性的研究进展[J/OL]. 中华胃肠内镜电子杂志, 2024, 11(03): 200-203.
阅读次数
全文


摘要