Innate immune cells in acute and chronic kidney disease

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Innate immune cells in acute and chronic kidney disease
  • Levin, A. et al. Executive summary of the KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease: known knowns and known unknowns. Kidney Int. 105, 684–701 (2024).

    Article 
    PubMed 

    Google Scholar 

  • Collaboration, G. B. D. C. K. D. Global, regional, and national burden of chronic kidney disease, 1990-2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet 395, 709–733 (2020).

    Article 

    Google Scholar 

  • Kidney Disease: Improving Global Outcomes (KDIGO) acute kidney injury work group. KDIGO clinical practice guideline for acute kidney injury. Kidney Int. Suppl. 2, 1–138 (2012).

  • Hoste, E. A. J. et al. Global epidemiology and outcomes of acute kidney injury. Nat. Rev. Nephrol. 14, 607–625 (2018).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Kellum, J. A. et al. Acute kidney injury. Nat. Rev. Dis. Prim. 7, 52 (2021).

    Article 
    PubMed 

    Google Scholar 

  • Levey, A. S. et al. Nomenclature for kidney function and disease: report of a Kidney Disease: Improving Global Outcomes (KDIGO) Consensus Conference. Kidney Int. 97, 1117–1129 (2020).

    Article 
    PubMed 

    Google Scholar 

  • Chawla, L. S., Eggers, P. W., Star, R. A. & Kimmel, P. L. Acute kidney injury and chronic kidney disease as interconnected syndromes. N. Engl. J. Med. 371, 58–66 (2014).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Levey, A. S. Defining AKD: the spectrum of AKI, AKD, and CKD. Nephron 146, 302–305 (2022).

    Article 
    PubMed 

    Google Scholar 

  • Coca, S. G., Singanamala, S. & Parikh, C. R. Chronic kidney disease after acute kidney injury: a systematic review and meta-analysis. Kidney Int. 81, 442–448 (2012).

    Article 
    PubMed 

    Google Scholar 

  • James, M. T. et al. Incidence and prognosis of acute kidney diseases and disorders using an integrated approach to laboratory measurements in a universal health care system. JAMA Netw. Open. 2, e191795 (2019).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

  • O’Neal, J. B., Shaw, A. D. & Billings, F. T. t. Acute kidney injury following cardiac surgery: current understanding and future directions. Crit. Care 20, 187 (2016).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Speer, T., Dimmeler, S., Schunk, S. J., Fliser, D. & Ridker, P. M. Targeting innate immunity-driven inflammation in CKD and cardiovascular disease. Nat. Rev. Nephrol. 18, 762–778 (2022).

    Article 
    PubMed 

    Google Scholar 

  • Ouyang, Q. et al. Depleting profibrotic macrophages using bioactivated in vivo assembly peptides ameliorates kidney fibrosis. Cell Mol. Immunol. 21, 826–841 (2024).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Hasegawa, S. et al. Activation of sympathetic signaling in macrophages blocks systemic inflammation and protects against renal ischemia-reperfusion injury. J. Am. Soc. Nephrol. 32, 1599–1615 (2021).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Tang, S. C. W. & Yiu, W. H. Innate immunity in diabetic kidney disease. Nat. Rev. Nephrol. 16, 206–222 (2020).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Wang, R., Wang, Y., Harris, D. C. H. & Cao, Q. Innate lymphoid cells in kidney diseases. Kidney Int. 99, 1077–1087 (2021).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Yao, W. et al. Single cell RNA sequencing identifies a unique inflammatory macrophage subset as a druggable target for alleviating acute kidney injury. Adv. Sci. 9, e2103675 (2022).

    Article 

    Google Scholar 

  • Dahlin, J. S. et al. KIT signaling is dispensable for human mast cell progenitor development. Blood 130, 1785–1794 (2017).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Cantoni, C. et al. Human NK cells and cancer. Oncoimmunology 13, 2378520 (2024).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Godfrey, D. I., Koay, H. F., McCluskey, J. & Gherardin, N. A. The biology and functional importance of MAIT cells. Nat. Immunol. 20, 1110–1128 (2019).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Paludan, S. R., Pradeu, T., Masters, S. L. & Mogensen, T. H. Constitutive immune mechanisms: mediators of host defence and immune regulation. Nat. Rev. Immunol. 21, 137–150 (2021).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Lazarov, T., Juarez-Carreno, S., Cox, N. & Geissmann, F. Physiology and diseases of tissue-resident macrophages. Nature 618, 698–707 (2023).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Mantovani, A. & Garlanda, C. Humoral innate immunity and acute-phase proteins. N. Engl. J. Med. 388, 439–452 (2023).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Li, D. & Wu, M. Pattern recognition receptors in health and diseases. Signal. Transduct. Target. Ther. 6, 291 (2021).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Ma, M., Jiang, W. & Zhou, R. DAMPs and DAMP-sensing receptors in inflammation and diseases. Immunity 57, 752–771 (2024).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Christgen, S., Place, D. E. & Kanneganti, T. D. Toward targeting inflammasomes: insights into their regulation and activation. Cell Res. 30, 315–327 (2020).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Xiao, L., Magupalli, V. G. & Wu, H. Cryo-EM structures of the active NLRP3 inflammasome disc. Nature 613, 595–600 (2023).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Fu, J. & Wu, H. Structural mechanisms of NLRP3 inflammasome assembly and activation. Annu. Rev. Immunol. 41, 301–316 (2023).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Hsu, C. G., Li, W., Sowden, M., Chavez, C. L. & Berk, B. C. Pnpt1 mediates NLRP3 inflammasome activation by MAVS and metabolic reprogramming in macrophages. Cell Mol. Immunol. 20, 131–142 (2023).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Gaidt, M. M. et al. Human monocytes engage an alternative inflammasome pathway. Immunity 44, 833–846 (2016).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Guzik, T. J., Nosalski, R., Maffia, P. & Drummond, G. R. Immune and inflammatory mechanisms in hypertension. Nat. Rev. Cardiol. 21, 396–416 (2024).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Saranya, G. R. & Viswanathan, P. Gut microbiota dysbiosis in AKI to CKD transition. Biomed. Pharmacother. 161, 114447 (2023).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Zhou, X. et al. Gut microbiota dysbiosis in hyperuricaemia promotes renal injury through the activation of NLRP3 inflammasome. Microbiome 12, 109 (2024).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Barratt, J. et al. IgA nephropathy: the lectin pathway and implications for targeted therapy. Kidney Int. 104, 254–264 (2023).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Tanaka, S. et al. Vascular adhesion protein-1 enhances neutrophil infiltration by generation of hydrogen peroxide in renal ischemia/reperfusion injury. Kidney Int. 92, 154–164 (2017).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Deng, B. et al. The leukotriene B4-leukotriene B4 receptor axis promotes cisplatin-induced acute kidney injury by modulating neutrophil recruitment. Kidney Int. 92, 89–100 (2017).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Ryan, J., Kanellis, J., Blease, K., Ma, F. Y. & Nikolic-Paterson, D. J. Spleen tyrosine kinase signaling promotes myeloid cell recruitment and kidney damage after renal ischemia/reperfusion injury. Am. J. Pathol. 186, 2032–2042 (2016).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Petr, V. & Thurman, J. M. The role of complement in kidney disease. Nat. Rev. Nephrol. 19, 771–787 (2023).

    Article 
    PubMed 

    Google Scholar 

  • Meissner, M., Viehmann, S. F. & Kurts, C. DAMPening sterile inflammation of the kidney. Kidney Int. 95, 489–491 (2019).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Vazquez-Carballo, C. et al. Toll-like receptors in acute kidney injury. Int J Mol Sci 22, 816 (2021).

  • Huang, X., Yu, Q., Zhang, L. & Jiang, Z. Research progress on Mincle as a multifunctional receptor. Int. Immunopharmacol. 114, 109467 (2023).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Lv, L. L. et al. The pattern recognition receptor, Mincle, is essential for maintaining the M1 macrophage phenotype in acute renal inflammation. Kidney Int. 91, 587–602 (2017).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Wang, C. et al. Mincle receptor in macrophage and neutrophil contributes to the unresolved inflammation during the transition from acute kidney injury to chronic kidney disease. Front. Immunol. 15, 1385696 (2024).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Raup-Konsavage, W. M. et al. Neutrophil peptidyl arginine deiminase-4 has a pivotal role in ischemia/reperfusion-induced acute kidney injury. Kidney Int. 93, 365–374 (2018).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Nakazawa, D. et al. Histones and neutrophil extracellular traps enhance tubular necrosis and remote organ injury in ischemic AKI. J. Am. Soc. Nephrol. 28, 1753–1768 (2017).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Chen, Z. et al. GSDMD and GSDME synergy in the transition of acute kidney injury to chronic kidney disease. Nephrol. Dial. Transpl. 39, 1344–1359 (2024).

    Article 
    CAS 

    Google Scholar 

  • Loh, W. & Vermeren, S. Anti-inflammatory neutrophil functions in the resolution of inflammation and tissue repair. Cells 11, 4076 (2022).

  • Suchitha, G. P., Devasahayam Arokia Balaya, R., Prasad, T. S. K. & Dagamajalu, S. A signaling network map of Lipoxin (LXA4): an anti-inflammatory molecule. Inflamm. Res. 73, 1099–1106 (2024).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Nakazawa, D., Masuda, S., Tomaru, U. & Ishizu, A. Pathogenesis and therapeutic interventions for ANCA-associated vasculitis. Nat. Rev. Rheumatol. 15, 91–101 (2019).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Shen, J. et al. Gasdermin D deficiency aborts myeloid calcium influx to drive granulopoiesis in lupus nephritis. Cell Commun. Signal. 22, 308 (2024).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Ryan, J. et al. Spleen tyrosine kinase promotes acute neutrophil-mediated glomerular injury via activation of JNK and p38 MAPK in rat nephrotoxic serum nephritis. Lab. Invest. 91, 1727–1738 (2011).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Ryan, J. et al. Myeloid cell-mediated renal injury in rapidly progressive glomerulonephritis depends upon spleen tyrosine kinase. J. Pathol. 238, 10–20 (2016).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Caster, D. J., Powell, D. W., Miralda, I., Ward, R. A. & McLeish, K. R. Re-examining neutrophil participation in GN. J. Am. Soc. Nephrol. 28, 2275–2289 (2017).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Pieterse, E. et al. Cleaved N-terminal histone tails distinguish between NADPH oxidase (NOX)-dependent and NOX-independent pathways of neutrophil extracellular trap formation. Ann. Rheum. Dis. 77, 1790–1798 (2018).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Thakur, M. et al. NETs-induced thrombosis impacts on cardiovascular and chronic kidney disease. Circ. Res. 132, 933–949 (2023).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • van der Linden, M. et al. Neutrophil extracellular trap release is associated with antinuclear antibodies in systemic lupus erythematosus and anti-phospholipid syndrome. Rheumatology 57, 1228–1234 (2018).

    Article 
    PubMed 

    Google Scholar 

  • Frangou, E. et al. REDD1/autophagy pathway promotes thromboinflammation and fibrosis in human systemic lupus erythematosus (SLE) through NETs decorated with tissue factor (TF) and interleukin-17A (IL-17A). Ann. Rheum. Dis. 78, 238–248 (2019).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Ueda, Y. et al. Transcription factor Nrf2 activation regulates NETosis, endothelial injury, and kidney disease in myeloperoxidase-positive antineutrophil cytoplasmic antibody-associated vasculitis. Kidney Int. 105, 1291–1305 (2024).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Kienhofer, D. et al. Experimental lupus is aggravated in mouse strains with impaired induction of neutrophil extracellular traps. JCI Insight 2, e92920 (2017).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Miao, N. et al. Oxidized mitochondrial DNA induces gasdermin D oligomerization in systemic lupus erythematosus. Nat. Commun. 14, 872 (2023).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Liu, F. et al. Distinct fate, dynamics and niches of renal macrophages of bone marrow or embryonic origins. Nat. Commun. 11, 2280 (2020).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Anders, H. J. & Ryu, M. Renal microenvironments and macrophage phenotypes determine progression or resolution of renal inflammation and fibrosis. Kidney Int. 80, 915–925 (2011).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Zhang, Y. L. et al. Identification of a novel ECM remodeling macrophage subset in AKI to CKD transition by integrative spatial and single-cell analysis. Adv. Sci. 11, e2309752 (2024).

    Article 

    Google Scholar 

  • Tang, P. M., Nikolic-Paterson, D. J. & Lan, H. Y. Macrophages: versatile players in renal inflammation and fibrosis. Nat. Rev. Nephrol. 15, 144–158 (2019).

    Article 
    PubMed 

    Google Scholar 

  • Ferenbach, D. A. et al. Macrophage/monocyte depletion by clodronate, but not diphtheria toxin, improves renal ischemia/reperfusion injury in mice. Kidney Int. 82, 928–933 (2012).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Culemann, S. et al. Stunning of neutrophils accounts for the anti-inflammatory effects of clodronate liposomes. J. Exp. Med. 220, e20220525 (2023).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Tan, R. Z. et al. Neuropeptide Y protects kidney from acute kidney injury by inactivating M1 macrophages via the Y1R-NF-κB-Mincle-dependent mechanism. Int. J. Biol. Sci. 19, 521–536 (2023).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Huang, W. et al. JAML promotes acute kidney injury mainly through a macrophage-dependent mechanism. JCI Insight 7, e158571 (2022).

  • Li, S. et al. Peroxiredoxin 1 aggravates acute kidney injury by promoting inflammation through Mincle/Syk/NF-κB signaling. Kidney Int. 104, 305–323 (2023).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Yuan, L. et al. Macrophage-derived exosomal miR-195a-5p impairs tubular epithelial cells mitochondria in acute kidney injury mice. FASEB J. 37, e22691 (2023).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Jiao, Y. et al. Exosomal PGE2 from M2 macrophages inhibits neutrophil recruitment and NET formation through lipid mediator class switching in sepsis. J. Biomed. Sci. 30, 62 (2023).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Li, J. H. et al. Macrophage migration inhibitory factor promotes renal injury induced by ischemic reperfusion. J. Cell Mol. Med. 23, 3867–3877 (2019).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Li, T. et al. Downregulation of macrophage migration inhibitory factor attenuates NLRP3 inflammasome mediated pyroptosis in sepsis-induced AKI. Cell Death Discov. 8, 61 (2022).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Stoppe, C. et al. The protective role of macrophage migration inhibitory factor in acute kidney injury after cardiac surgery. Sci. Transl. Med. 10, eaan4886 (2018).

    Article 
    PubMed 

    Google Scholar 

  • Huen, S. C. & Cantley, L. G. Macrophages in renal injury and repair. Annu. Rev. Physiol. 79, 449–469 (2017).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Zhang, M. Z. et al. CSF-1 signaling mediates recovery from acute kidney injury. J. Clin. Invest. 122, 4519–4532 (2012).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Shin, N. S. et al. Arginase-1 is required for macrophage-mediated renal tubule regeneration. J. Am. Soc. Nephrol. 33, 1077–1086 (2022).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Lech, M. et al. Macrophage phenotype controls long-term AKI outcomes-kidney regeneration versus atrophy. J. Am. Soc. Nephrol. 25, 292–304 (2014).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Kim, S. R. et al. Progressive cellular senescence mediates renal dysfunction in ischemic nephropathy. J. Am. Soc. Nephrol. 32, 1987–2004 (2021).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Xu, L., Guo, J., Moledina, D. G. & Cantley, L. G. Immune-mediated tubule atrophy promotes acute kidney injury to chronic kidney disease transition. Nat. Commun. 13, 4892 (2022).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Kormann, R. et al. Periostin promotes cell proliferation and macrophage polarization to drive repair after AKI. J. Am. Soc. Nephrol. 31, 85–100 (2020).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Huen, S. C., Moeckel, G. W. & Cantley, L. G. Macrophage-specific deletion of transforming growth factor-beta1 does not prevent renal fibrosis after severe ischemia-reperfusion or obstructive injury. Am. J. Physiol. Renal Physiol. 305, F477–F484 (2013).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Belliere, J. et al. Specific macrophage subtypes influence the progression of rhabdomyolysis-induced kidney injury. J. Am. Soc. Nephrol. 26, 1363–1377 (2015).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Meng, X. M. et al. Inflammatory macrophages can transdifferentiate into myofibroblasts during renal fibrosis. Cell Death Dis. 7, e2495 (2016).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Chung, J. Y. et al. Immunodynamics of macrophages in renal fibrosis. Integr. Med. Nephrol. Androl. 10, e00001 (2023).

    Article 

    Google Scholar 

  • Eardley, K. S. et al. The relationship between albuminuria, MCP-1/CCL2, and interstitial macrophages in chronic kidney disease. Kidney Int. 69, 1189–1197 (2006).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Xie, D. et al. Intensity of macrophage infiltration in glomeruli predicts response to immunosuppressive therapy in patients with IgA nephropathy. J. Am. Soc. Nephrol. 32, 3187–3196 (2021).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Ikezumi, Y. et al. The sialoadhesin (CD169) expressing a macrophage subset in human proliferative glomerulonephritis. Nephrol. Dial. Transpl. 20, 2704–2713 (2005).

    Article 
    CAS 

    Google Scholar 

  • Ikezumi, Y. et al. Identification of alternatively activated macrophages in new-onset paediatric and adult immunoglobulin A nephropathy: potential role in mesangial matrix expansion. Histopathology 58, 198–210 (2011).

    Article 
    PubMed 

    Google Scholar 

  • Mejia-Vilet, J. M. et al. Urinary soluble CD163: a novel noninvasive biomarker of activity for lupus nephritis. J. Am. Soc. Nephrol. 31, 1335–1347 (2020).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Aendekerk, J. P. et al. CD163 and CD206 expression define distinct macrophage subsets involved in active ANCA-associated glomerulonephritis. J. Autoimmun. 133, 102914 (2022).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Ikezumi, Y. et al. Steroid treatment promotes an M2 anti-inflammatory macrophage phenotype in childhood lupus nephritis. Pediatr. Nephrol. 36, 349–359 (2021).

    Article 
    PubMed 

    Google Scholar 

  • Han, Y., Ma, F. Y., Tesch, G. H., Manthey, C. L. & Nikolic-Paterson, D. J. Role of macrophages in the fibrotic phase of rat crescentic glomerulonephritis. Am. J. Physiol. Renal Physiol. 304, F1043–F1053 (2013).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Lim, A. K. et al. Antibody blockade of c-fms suppresses the progression of inflammation and injury in early diabetic nephropathy in obese db/db mice. Diabetologia 52, 1669–1679 (2009).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Chalmers, S. A. et al. Macrophage depletion ameliorates nephritis induced by pathogenic antibodies. J. Autoimmun. 57, 42–52 (2015).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Meng, X. M., Nikolic-Paterson, D. J. & Lan, H. Y. Inflammatory processes in renal fibrosis. Nat. Rev. Nephrol. 10, 493–503 (2014).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Peter, J. K. et al. Renal macrophages induce hypertension and kidney fibrosis in Angiotensin II salt mice model. Biochem. Biophys. Res. Commun. 715, 149997 (2024).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Swenson-Fields, K. I. et al. Macrophages promote polycystic kidney disease progression. Kidney Int. 83, 855–864 (2013).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Chow, F. Y. et al. Monocyte chemoattractant protein-1 promotes the development of diabetic renal injury in streptozotocin-treated mice. Kidney Int. 69, 73–80 (2006).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Chen, J. et al. Single-cell RNA sequencing identified novel Nr4a1+ Ear2+ anti-inflammatory macrophage phenotype under myeloid-TLR4 dependent regulation in anti-glomerular basement membrane (GBM) crescentic glomerulonephritis (cGN). Adv. Sci. 9, e2200668 (2022).

    Article 

    Google Scholar 

  • Yang, F. et al. Regulatory role and mechanisms of myeloid TLR4 in anti-GBM glomerulonephritis. Cell Mol. Life Sci. 78, 6721–6734 (2021).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Kluger, M. A. et al. Leukocyte-derived MMP9 is crucial for the recruitment of proinflammatory macrophages in experimental glomerulonephritis. Kidney Int. 83, 865–877 (2013).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Paust, H. J. et al. CD4+ T cells produce GM-CSF and drive immune-mediated glomerular disease by licensing monocyte-derived cells to produce MMP12. Sci. Transl. Med. 15, eadd6137 (2023).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Ikezumi, Y., Hurst, L. A., Masaki, T., Atkins, R. C. & Nikolic-Paterson, D. J. Adoptive transfer studies demonstrate that macrophages can induce proteinuria and mesangial cell proliferation. Kidney Int. 63, 83–95 (2003).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Ikezumi, Y., Atkins, R. C. & Nikolic-Paterson, D. J. Interferon-γ augments acute macrophage-mediated renal injury via a glucocorticoid-sensitive mechanism. J. Am. Soc. Nephrol. 14, 888–898 (2003).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Shi, M. et al. Single-cell RNA sequencing shows the immune cell landscape in the kidneys of patients with idiopathic membranous nephropathy. Front. Immunol. 14, 1203062 (2023).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Fu, J. et al. The single-cell landscape of kidney immune cells reveals transcriptional heterogeneity in early diabetic kidney disease. Kidney Int. 102, 1291–1304 (2022).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Conway, B. R. et al. Kidney single-cell atlas reveals myeloid heterogeneity in progression and regression of kidney disease. J. Am. Soc. Nephrol. 31, 2833–2854 (2020).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Lu, J. et al. Discrete functions of M2a and M2c macrophage subsets determine their relative efficacy in treating chronic kidney disease. Kidney Int. 84, 745–755 (2013).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Lu, J. et al. M2c macrophages protect mice from adriamycin-induced nephropathy by upregulating CD62L in Tregs. Mediators Inflamm. 2022, 1153300 (2022).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Ding, N. et al. Macrophage migration inhibitory factor levels are associated with disease activity and possible complications in membranous nephropathy. Sci. Rep. 12, 18558 (2022).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Bruchfeld, A., Wendt, M. & Miller, E. J. Macrophage migration inhibitory factor in clinical kidney disease. Front. Immunol. 7, 8 (2016).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Jankauskas, S. S., Wong, D. W. L., Bucala, R., Djudjaj, S. & Boor, P. Evolving complexity of MIF signaling. Cell Signal. 57, 76–88 (2019).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Yang, N. et al. Reversal of established rat crescentic glomerulonephritis by blockade of macrophage migration inhibitory factor (MIF): potential role of MIF in regulating glucocorticoid production. Mol. Med. 4, 413–424 (1998).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Leng, L. et al. A small-molecule macrophage migration inhibitory factor antagonist protects against glomerulonephritis in lupus-prone NZB/NZW F1 and MRL/lpr mice. J. Immunol. 186, 527–538 (2011).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Schunk, S. J., Floege, J., Fliser, D. & Speer, T. WNT-β-catenin signalling — a versatile player in kidney injury and repair. Nat. Rev. Nephrol. 17, 172–184 (2021).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Tian, Y. et al. Myeloid-derived Wnts play an indispensible role in macrophage and fibroblast activation and kidney fibrosis. Int. J. Biol. Sci. 20, 2310–2322 (2024).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Cohen, C. et al. WNT-dependent interaction between inflammatory fibroblasts and FOLR2+ macrophages promotes fibrosis in chronic kidney disease. Nat. Commun. 15, 743 (2024).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Lin, S. L. et al. Macrophage Wnt7b is critical for kidney repair and regeneration. Proc. Natl Acad. Sci. USA 107, 4194–4199 (2010).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Song, Y. et al. Macrophage-derived exosomes as advanced therapeutics for inflammation: current progress and future perspectives. Int. J. Nanomed. 19, 1597–1627 (2024).

    Article 
    CAS 

    Google Scholar 

  • Liu, Y. et al. Macrophage-derived exosomes promote activation of NLRP3 inflammasome and autophagy deficiency of mesangial cells in diabetic nephropathy. Life Sci. 330, 121991 (2023).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Zhao, J., Chen, J., Zhu, W., Qi, X. M. & Wu, Y. G. Exosomal miR-7002-5p derived from highglucose-induced macrophages suppresses autophagy in tubular epithelial cells by targeting Atg9b. FASEB J. 36, e22501 (2022).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Li, Q. et al. High-phosphate-stimulated macrophage-derived exosomes promote vascular calcification via let-7b-5p/TGFBR1 axis in chronic kidney disease. Cells 12, 161 (2022).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Huang, H. et al. M2 macrophage-derived exosomal miR-25-3p improves high glucose-induced podocytes injury through activation autophagy via inhibiting DUSP1 expression. IUBMB Life 72, 2651–2662 (2020).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Yin, Q. et al. Macrophage-derived exosomes promote telomere fragility and senescence in tubular epithelial cells by delivering miR-155. Cell Commun. Signal. 22, 357 (2024).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Wang, S. et al. TGF-β/Smad3 signalling regulates the transition of bone marrow-derived macrophages into myofibroblasts during tissue fibrosis. Oncotarget 7, 8809–8822 (2016).

    Article 
    PubMed 

    Google Scholar 

  • Lan, H. Y. Macrophage-myofibroblast transition in kidney disease. Integr. Med. Nephrol. Androl. 9, 12 (2022).

    Article 

    Google Scholar 

  • Tang, P. M. et al. Neural transcription factor Pou4f1 promotes renal fibrosis via macrophage-myofibroblast transition. Proc. Natl Acad. Sci. USA 117, 20741–20752 (2020).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Wang, Y. Y. et al. Macrophage-to-myofibroblast transition contributes to interstitial fibrosis in chronic renal allograft injury. J. Am. Soc. Nephrol. 28, 2053–2067 (2017).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Kramann, R. et al. Parabiosis and single-cell RNA sequencing reveal a limited contribution of monocytes to myofibroblasts in kidney fibrosis. JCI Insight 3, e99561 (2018).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Chen, J. et al. P2Y12 inhibitor clopidogrel inhibits renal fibrosis by blocking macrophage-to-myofibroblast transition. Mol. Ther. 30, 3017–3033 (2022).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Kuppe, C. et al. Decoding myofibroblast origins in human kidney fibrosis. Nature 589, 281–286 (2021).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Kurts, C., Ginhoux, F. & Panzer, U. Kidney dendritic cells: fundamental biology and functional roles in health and disease. Nat. Rev. Nephrol. 16, 391–407 (2020).

    Article 
    PubMed 

    Google Scholar 

  • Tadagavadi, R. K. & Reeves, W. B. Renal dendritic cells ameliorate nephrotoxic acute kidney injury. J. Am. Soc. Nephrol. 21, 53–63 (2010).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Lv, D. et al. Advances in understanding of dendritic cell in the pathogenesis of acute kidney injury. Front. Immunol. 15, 1294807 (2024).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Dai, H., Thomson, A. W. & Rogers, N. M. Dendritic cells as sensors, mediators, and regulators of ischemic injury. Front. Immunol. 10, 2418 (2019).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Li, J. S. Y. et al. Tolerogenic dendritic cells protect against acute kidney injury. Kidney Int. 104, 492–507 (2023).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Qu, J. et al. Hypoxia-inducible factor 2ɑ attenuates renal ischemia-reperfusion injury by suppressing CD36-mediated lipid accumulation in dendritic cells in a mouse model. J. Am. Soc. Nephrol. 34, 73–87 (2023).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Jia, P. et al. Depletion of miR-21 in dendritic cells aggravates renal ischemia-reperfusion injury. FASEB J. 34, 11729–11740 (2020).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Li, L. et al. Dendritic cells tolerized with adenosine A2AR agonist attenuate acute kidney injury. J Clin. Invest. 122, 3931–3942 (2012).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Li, J., Thomson, A. W. & Rogers, N. M. Myeloid and mesenchymal stem cell therapies for solid organ transplant tolerance. Transplantation 105, e303–e321 (2021).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Chen, W. et al. Single-cell profiling reveals kidney CD163+ dendritic cell participation in human lupus nephritis. Ann. Rheum. Dis. 83, 608–623 (2024).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Kassianos, A. J. et al. Increased tubulointerstitial recruitment of human CD141hi CLEC9A+ and CD1c+ myeloid dendritic cell subsets in renal fibrosis and chronic kidney disease. Am. J. Physiol. Renal Physiol. 305, F1391–F1401 (2013).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Arazi, A. et al. The immune cell landscape in kidneys of patients with lupus nephritis. Nat. Immunol. 20, 902–914 (2019).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Wang, Y. et al. High renal DC-SIGN+ cell density is associated with severe renal lesions and poor prognosis in patients with immunoglobulin A nephropathy. Histopathology 74, 744–758 (2019).

    Article 
    PubMed 

    Google Scholar 

  • Chen, T. et al. Conventional type 1 dendritic cells (cDC1) in human kidney diseases: clinico-pathological correlations. Front. Immunol. 12, 635212 (2021).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Zheng, D. et al. Lipopolysaccharide-pretreated plasmacytoid dendritic cells ameliorate experimental chronic kidney disease. Kidney Int. 81, 892–902 (2012).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Cao, Q. et al. CD103+ dendritic cells elicit CD8+ T cell responses to accelerate kidney injury in adriamycin nephropathy. J. Am. Soc. Nephrol. 27, 1344–1360 (2016).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Wang, R. et al. Flt3 inhibition alleviates chronic kidney disease by suppressing CD103+ dendritic cell-mediated T cell activation. Nephrol. Dial. Transpl. 34, 1853–1863 (2019).

    Article 
    CAS 

    Google Scholar 

  • Brahler, S. et al. Opposing roles of dendritic cell subsets in experimental GN. J. Am. Soc. Nephrol. 29, 138–154 (2018).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • McKenzie, A. N. J., Spits, H. & Eberl, G. Innate lymphoid cells in inflammation and immunity. Immunity 41, 366–374 (2014).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Huang, Q. et al. IL-25 elicits innate lymphoid cells and multipotent progenitor type 2 cells that reduce renal ischemic/reperfusion injury. J. Am. Soc. Nephrol. 26, 2199–2211 (2015).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Cao, Q. et al. Potentiating tissue-resident type 2 innate lymphoid cells by IL-33 to prevent renal ischemia-reperfusion injury. J. Am. Soc. Nephrol. 29, 961–976 (2018).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Cameron, G. J. M. et al. Group 2 innate lymphoid cells are redundant in experimental renal ischemia-reperfusion injury. Front. Immunol. 10, 826 (2019).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Akcay, A. et al. IL-33 exacerbates acute kidney injury. J. Am. Soc. Nephrol. 22, 2057–2067 (2011).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Sehnine, M. et al. IL-33 receptor ST2 deficiency attenuates renal ischaemia-reperfusion injury in euglycaemic, but not streptozotocin-induced hyperglycaemic mice. Diabetes Metab. 44, 55–60 (2018).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Ferhat, M. et al. Endogenous IL-33 contributes to kidney ischemia-reperfusion injury as an alarmin. J. Am. Soc. Nephrol. 29, 1272–1288 (2018).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Vely, F. et al. Evidence of innate lymphoid cell redundancy in humans. Nat. Immunol. 17, 1291–1299 (2016).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Liu, G. Y. et al. Expansion of group 2 innate lymphoid cells in patients with end-stage renal disease and their clinical significance. J. Immunol. 205, 36–44 (2020).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Ryu, S. et al. Reduction of circulating innate lymphoid cell progenitors results in impaired cytokine production by innate lymphoid cells in patients with lupus nephritis. Arthritis Res. Ther. 22, 63 (2020).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Liang, Z. et al. Intestinal CXCR6+ ILC3s migrate to the kidney and exacerbate renal fibrosis via IL-23 receptor signaling enhanced by PD-1 expression. Immunity 57, 1306–1323 e1308 (2024).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Nagashima, R. et al. Group2 innate lymphoid cells ameliorate renal fibrosis and dysfunction associated with adenine-induced CKD. Cell Immunol. 401-402, 104828 (2024).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Turner, J. E., Rickassel, C., Healy, H. & Kassianos, A. J. Natural killer cells in kidney health and disease. Front. Immunol. 10, 587 (2019).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Kim, H. J. et al. Reverse signaling through the costimulatory ligand CD137L in epithelial cells is essential for natural killer cell-mediated acute tissue inflammation. Proc. Natl Acad. Sci. USA 109, E13–E22 (2012).

    CAS 
    PubMed 

    Google Scholar 

  • Victorino, F. et al. Tissue-resident NK cells mediate ischemic kidney injury and are not depleted by anti-asialo-GM1 antibody. J. Immunol. 195, 4973–4985 (2015).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Law, B. M. P. et al. Interferon-γ production by tubulointerstitial human CD56bright natural killer cells contributes to renal fibrosis and chronic kidney disease progression. Kidney Int. 92, 79–88 (2017).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Spada, R. et al. NKG2D ligand overexpression in lupus nephritis correlates with increased NK cell activity and differentiation in kidneys but not in the periphery. J. Leukoc. Biol. 97, 583–598 (2015).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Postol, E. et al. Long-term administration of IgG2a anti-NK1.1 monoclonal antibody ameliorates lupus-like disease in NZB/W mice in spite of an early worsening induced by an IgG2a-dependent BAFF/BLyS production. Immunology 125, 184–196 (2008).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Rickassel, C. et al. Conventional NK cells and type 1 innate lymphoid cells do not influence pathogenesis of experimental glomerulonephritis. J. Immunol. 208, 1585–1594 (2022).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Zheng, G. et al. NK cells do not mediate renal injury in murine adriamycin nephropathy. Kidney Int. 69, 1159–1165 (2006).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Vibhushan, S. et al. Mast cell chymase and kidney disease. Int. J. Mol. Sci. 22, 302 (2020).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Danelli, L. et al. Early phase mast cell activation determines the chronic outcome of renal ischemia-reperfusion injury. J. Immunol. 198, 2374–2382 (2017).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Summers, S. A. et al. Mast cells mediate acute kidney injury through the production of TNF. J. Am. Soc. Nephrol. 22, 2226–2236 (2011).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Tong, F., Luo, L. & Liu, D. Effect of intervention in mast cell function before reperfusion on renal ischemia-reperfusion injury in rats. Kidney Blood Press. Res. 41, 335–344 (2016).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Madjene, L. C. et al. Mast cell chymase protects against acute ischemic kidney injury by limiting neutrophil hyperactivation and recruitment. Kidney Int. 97, 516–527 (2020).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Owens, E. P. et al. Biomarkers and the role of mast cells as facilitators of inflammation and fibrosis in chronic kidney disease. Transl. Androl. Urol. 8, S175–S183 (2019).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Kim, D. H. et al. Mast cells decrease renal fibrosis in unilateral ureteral obstruction. Kidney Int. 75, 1031–1038 (2009).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Madjene, L. C. et al. Mast cells in renal inflammation and fibrosis: lessons learnt from animal studies. Mol. Immunol. 63, 86–93 (2015).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Lin, L., Gerth, A. J. & Peng, S. L. Susceptibility of mast cell-deficient W/Wv mice to pristane-induced experimental lupus nephritis. Immunol. Lett. 91, 93–97 (2004).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Charles, N., Hardwick, D., Daugas, E., Illei, G. G. & Rivera, J. Basophils and the T helper 2 environment can promote the development of lupus nephritis. Nat. Med. 16, 701–707 (2010).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Doke, T. et al. Single-cell analysis identifies the interaction of altered renal tubules with basophils orchestrating kidney fibrosis. Nat. Immunol. 23, 947–959 (2022).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Hattori, K. et al. Interstitial eosinophilic aggregates and kidney outcome in patients with CKD. Clin. J. Am. Soc. Nephrol. 18, 1563–1572 (2023).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Yang, S. H. et al. Sulfatide-reactive natural killer T cells abrogate ischemia-reperfusion injury. J. Am. Soc. Nephrol. 22, 1305–1314 (2011).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Uchida, T. et al. Activated natural killer T cells in mice induce acute kidney injury with hematuria through possibly common mechanisms shared by human CD56+ T cells. Am. J. Physiol. Renal Physiol. 315, F618–F627 (2018).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Law, B. M. P. et al. Human tissue-resident mucosal-associated invariant T (MAIT) cells in renal fibrosis and CKD. J. Am. Soc. Nephrol. 30, 1322–1335 (2019).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Gnirck, A. C. et al. Mucosal-associated invariant T cells contribute to suppression of inflammatory myeloid cells in immune-mediated kidney disease. Nat. Commun. 14, 7372 (2023).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Pal, S. K. et al. CD70-targeted allogeneic CAR T-cell therapy for advanced clear cell renal cell carcinoma. Cancer Discov. 14, 1176–1189 (2024).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Robinson, W. H. et al. Cutting-edge approaches to B-cell depletion in autoimmune diseases. Front. Immunol. 15, 1454747 (2024).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Vivarelli, M. et al. The role of complement in kidney disease: conclusions from a Kidney Disease: Improving Global Outcomes (KDIGO) controversies conference. Kidney Int. 106, 369–391 (2024).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Cao, M. et al. Eculizumab modifies outcomes in adults with atypical hemolytic uremic syndrome with acute kidney injury. Am. J. Nephrol. 48, 225–233 (2018).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Ruggenenti, P. et al. C5 convertase blockade in membranoproliferative glomerulonephritis: a single-arm clinical trial. Am. J. Kidney Dis. 74, 224–238 (2019).

    Article 
    CAS 

    Google Scholar 

  • Le Quintrec, M. et al. Patterns of clinical response to eculizumab in patients with C3 glomerulopathy. Am. J. Kidney Dis. 72, 84–92 (2018).

    Article 
    PubMed 

    Google Scholar 

  • Ariceta, G. et al. The long-acting C5 inhibitor, ravulizumab, is effective and safe in pediatric patients with atypical hemolytic uremic syndrome naive to complement inhibitor treatment. Kidney Int. 100, 225–237 (2021).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Jayne, D. R. W., Merkel, P. A., Schall, T. J., Bekker, P. & Group, A. S. Avacopan for the treatment of ANCA-associated vasculitis. N. Engl. J. Med. 384, 599–609 (2021).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Wooden, B., Tarragon, B., Navarro-Torres, M. & Bomback, A. S. Complement inhibitors for kidney disease. Nephrol. Dial. Transpl. 38, ii29–ii39 (2023).

    Article 

    Google Scholar 

  • Zhang, H. et al. Results of a randomized double-blind placebo-controlled Phase 2 study propose iptacopan as an alternative complement pathway inhibitor for IgA nephropathy. Kidney Int. 105, 189–199 (2024).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Bomback, A. S. et al. Alternative complement pathway inhibition with iptacopan for the treatment of C3 glomerulopathy-study design of the APPEAR-C3G trial. Kidney Int. Rep. 7, 2150–2159 (2022).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Ito, S. et al. Effects of a CCR2 antagonist on macrophages and Toll-like receptor 9 expression in a mouse model of diabetic nephropathy. Am. J. Physiol. Renal Physiol. 321, F757–F770 (2021).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Sullivan, T. et al. CCR2 antagonist CCX140-B provides renal and glycemic benefits in diabetic transgenic human CCR2 knockin mice. Am. J. Physiol. Renal Physiol. 305, F1288–F1297 (2013).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Kashyap, S. et al. Blockade of CCR2 reduces macrophage influx and development of chronic renal damage in murine renovascular hypertension. Am. J. Physiol. Renal Physiol. 310, F372–F384 (2016).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Wang, X., Xie, L. & Liu, C. CCR2 antagonist attenuates calcium oxalate-induced kidney oxidative stress and inflammation by regulating macrophage activation. Exp. Anim. 73, 211–222 (2024).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • de Zeeuw, D. et al. The effect of CCR2 inhibitor CCX140-B on residual albuminuria in patients with type 2 diabetes and nephropathy: a randomised trial. Lancet Diabetes Endocrinol. 3, 687–696 (2015).

    Article 
    PubMed 

    Google Scholar 

  • Tesch, G. H., Pullen, N., Jesson, M. I., Schlerman, F. J. & Nikolic-Paterson, D. J. Combined inhibition of CCR2 and ACE provides added protection against progression of diabetic nephropathy in Nos3-deficient mice. Am. J. Physiol. Renal Physiol. 317, F1439–F1449 (2019).

    Article 
    PubMed 

    Google Scholar 

  • Gale, J. D. et al. Effect of PF-04634817, an Oral CCR2/5 chemokine receptor antagonist, on albuminuria in adults with overt diabetic nephropathy. Kidney Int. Rep. 3, 1316–1327 (2018).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Gubernatorova, E. O. et al. Targeting inerleukin-6 for renoprotection. Front. Immunol. 15, 1502299 (2024).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Doberer, K. et al. A randomized clinical trial of anti-IL-6 antibody clazakizumab in late antibody-mediated kidney transplant rejection. J. Am. Soc. Nephrol. 32, 708–722 (2021).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Borski, A. et al. Anti-interleukin-6 antibody clazakizumab in antibody-mediated renal allograft rejection: accumulation of antibody-neutralized interleukin-6 without signs of proinflammatory rebound phenomena. Transplantation 107, 495–503 (2023).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Lan, H. Y., Nikolic-Paterson, D. J., Zarama, M., Vannice, J. L. & Atkins, R. C. Suppression of experimental crescentic glomerulonephritis by the interleukin-1 receptor antagonist. Kidney Int. 43, 479–485 (1993).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Ridker, P. M. et al. Inhibition of interleukin-1β by canakinumab and cardiovascular outcomes in patients with chronic kidney disease. J. Am. Coll. Cardiol. 71, 2405–2414 (2018).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Tam, F. W. K. et al. Randomized trial on the effect of an oral spleen tyrosine kinase inhibitor in the treatment of IgA nephropathy. Kidney Int. Rep. 8, 2546–2556 (2023).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Ramessur Chandran, S. et al. Inhibition of spleen tyrosine kinase reduces renal allograft injury in a rat model of acute antibody-mediated rejection in sensitized recipients. Transplantation 101, e240–e248 (2017).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Tempest-Roe, S. et al. Inhibition of spleen tyrosine kinase decreases donor specific antibody levels in a rat model of sensitization. Sci. Rep. 12, 3330 (2022).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • US National Library of Medicine. Clinicaltrials.gov. (2024).

  • Xue, C. et al. Evolving cognition of the JAK-STAT signaling pathway: autoimmune disorders and cancer. Signal. Transduct. Target. Ther. 8, 204 (2023).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Tuttle, K. R. et al. JAK1/JAK2 inhibition by baricitinib in diabetic kidney disease: results from a Phase 2 randomized controlled clinical trial. Nephrol. Dial. Transpl. 33, 1950–1959 (2018).

    Article 
    CAS 

    Google Scholar 

  • Li, J. et al. Blocking macrophage migration inhibitory factor protects against cisplatin-induced acute kidney injury in mice. Mol. Ther. 26, 2523–2532 (2018).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Ludwig-Portugall, I. et al. An NLRP3-specific inflammasome inhibitor attenuates crystal-induced kidney fibrosis in mice. Kidney Int. 90, 525–539 (2016).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Liu, Z. et al. NLRP3 inflammasome of renal tubular epithelial cells induces kidney injury in acute hemolytic transfusion reactions. Clin. Transl. Med. 11, e373 (2021).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Elsayed, M. S., Abu-Elsaad, N. M. & Nader, M. A. The NLRP3 inhibitor dapansutrile attenuates folic acid induced nephrotoxicity via inhibiting inflammasome/caspase-1/IL axis and regulating autophagy/proliferation. Life Sci. 285, 119974 (2021).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Zhang, X., Hu, L., Xu, S., Ye, C. & Chen, A. Erianin: a direct NLRP3 inhibitor with remarkable anti-inflammatory activity. Front. Immunol. 12, 739953 (2021).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Zhu, P. et al. Thiolutin, a selective NLRP3 inflammasome inhibitor, attenuates cyclophosphamide-induced impairment of sperm and fertility in mice. Immunopharmacol. Immunotoxicol. 46, 172–182 (2024).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Meng, X. M., Nikolic-Paterson, D. J. & Lan, H. Y. TGF-β: the master regulator of fibrosis. Nat. Rev. Nephrol. 12, 325–338 (2016).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Voelker, J. et al. Anti-TGF-β1 antibody therapy in patients with diabetic nephropathy. J. Am. Soc. Nephrol. 28, 953–962 (2017).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Zhang, Y., Meng, X. M., Huang, X. R. & Lan, H. Y. The preventive and therapeutic implication for renal fibrosis by targetting TGF-β/Smad3 signaling. Clin. Sci. 132, 1403–1415 (2018).

    Article 
    CAS 

    Google Scholar 

  • Wang, W. et al. SARS-CoV-2 N protein induces acute kidney injury via smad3-dependent G1 cell cycle arrest mechanism. Adv. Sci. 9, e2103248 (2022).

    Article 

    Google Scholar 

  • Wu, W. et al. Treatment with quercetin inhibits SARS-CoV-2 N protein-induced acute kidney injury by blocking Smad3-dependent G1 cell-cycle arrest. Mol. Ther. 31, 344–361 (2023).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Liang, L. et al. SARS-CoV-2 N protein induces acute kidney injury in diabetic mice via the Smad3-Ripk3/MLKL necroptosis pathway. Signal. Transduct. Target. Ther. 8, 147 (2023).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Wu, N. et al. Discovery of a novel selective water-soluble SMAD3 inhibitor as an antitumor agent. Bioorg. Med. Chem. Lett. 30, 127396 (2020).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Lv, L. L., Feng, Y., Tang, T. T. & Liu, B. C. New insight into the role of extracellular vesicles in kidney disease. J. Cell Mol. Med. 23, 731–739 (2019).

    Article 
    PubMed 

    Google Scholar 

  • Li, J. et al. Role of miRNAs in macrophage-mediated kidney injury. Pediatr. Nephrol. 39, 3397–3410 (2024).

    Article 
    PubMed 

    Google Scholar 

  • Chung, J. Y. et al. Smad3 is essential for polarization of tumor-associated neutrophils in non-small cell lung carcinoma. Nat. Commun. 14, 1794 (2023).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Johnnidis, J. B. et al. Regulation of progenitor cell proliferation and granulocyte function by microRNA-223. Nature 451, 1125–1129 (2008).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Oliveira, M. C. et al. Eosinophils protect from metabolic alterations triggered by obesity. Metabolism 146, 155613 (2023).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Chen, Y. et al. Basophil differentiation, heterogeneity, and functional implications. Trends Immunol. 45, 523–534 (2024).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Geissmann, F., Jung, S. & Littman, D. R. Blood monocytes consist of two principal subsets with distinct migratory properties. Immunity 19, 71–82 (2003).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • T’Jonck, W. & Bain, C. C. The role of monocyte-derived macrophages in the lung: it’s all about context. Int. J. Biochem. Cell Biol. 159, 106421 (2023).

    Article 
    PubMed 

    Google Scholar 

  • Palucka, K. & Banchereau, J. Cancer immunotherapy via dendritic cells. Nat. Rev. Cancer 12, 265–277 (2012).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Feng, J. et al. Clonal lineage tracing reveals shared origin of conventional and plasmacytoid dendritic cells. Immunity 55, 405–422.e11 (2022).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Vivier, E. et al. Innate lymphoid cells: 10 years on. Cell 174, 1054–1066 (2018).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Bryceson, Y. T. et al. Functional analysis of human NK cells by flow cytometry. Methods Mol. Biol. 612, 335–352 (2010).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Stabile, H., Fionda, C., Santoni, A. & Gismondi, A. Impact of bone marrow-derived signals on NK cell development and functional maturation. Cytokine Growth Factor. Rev. 42, 13–19 (2018).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Dhodapkar, M. V. & Kumar, V. Type II NKT cells and their emerging role in health and disease. J. Immunol. 198, 1015–1021 (2017).

    Article 
    CAS 
    PubMed 

    Google Scholar 

  • Waterholter, A., Wunderlich, M. & Turner, J. E. MAIT cells in immune-mediated tissue injury and repair. Eur. J. Immunol. 53, e2350483 (2023).

    Article 
    PubMed 

    Google Scholar 

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