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).
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).
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).
Google Scholar
Kellum, J. A. et al. Acute kidney injury. Nat. Rev. Dis. Prim. 7, 52 (2021).
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).
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).
Google Scholar
Levey, A. S. Defining AKD: the spectrum of AKI, AKD, and CKD. Nephron 146, 302–305 (2022).
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).
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).
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).
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).
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).
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).
Google Scholar
Tang, S. C. W. & Yiu, W. H. Innate immunity in diabetic kidney disease. Nat. Rev. Nephrol. 16, 206–222 (2020).
Google Scholar
Wang, R., Wang, Y., Harris, D. C. H. & Cao, Q. Innate lymphoid cells in kidney diseases. Kidney Int. 99, 1077–1087 (2021).
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).
Google Scholar
Dahlin, J. S. et al. KIT signaling is dispensable for human mast cell progenitor development. Blood 130, 1785–1794 (2017).
Google Scholar
Cantoni, C. et al. Human NK cells and cancer. Oncoimmunology 13, 2378520 (2024).
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).
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).
Google Scholar
Lazarov, T., Juarez-Carreno, S., Cox, N. & Geissmann, F. Physiology and diseases of tissue-resident macrophages. Nature 618, 698–707 (2023).
Google Scholar
Mantovani, A. & Garlanda, C. Humoral innate immunity and acute-phase proteins. N. Engl. J. Med. 388, 439–452 (2023).
Google Scholar
Li, D. & Wu, M. Pattern recognition receptors in health and diseases. Signal. Transduct. Target. Ther. 6, 291 (2021).
Google Scholar
Ma, M., Jiang, W. & Zhou, R. DAMPs and DAMP-sensing receptors in inflammation and diseases. Immunity 57, 752–771 (2024).
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).
Google Scholar
Xiao, L., Magupalli, V. G. & Wu, H. Cryo-EM structures of the active NLRP3 inflammasome disc. Nature 613, 595–600 (2023).
Google Scholar
Fu, J. & Wu, H. Structural mechanisms of NLRP3 inflammasome assembly and activation. Annu. Rev. Immunol. 41, 301–316 (2023).
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).
Google Scholar
Gaidt, M. M. et al. Human monocytes engage an alternative inflammasome pathway. Immunity 44, 833–846 (2016).
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).
Google Scholar
Saranya, G. R. & Viswanathan, P. Gut microbiota dysbiosis in AKI to CKD transition. Biomed. Pharmacother. 161, 114447 (2023).
Google Scholar
Zhou, X. et al. Gut microbiota dysbiosis in hyperuricaemia promotes renal injury through the activation of NLRP3 inflammasome. Microbiome 12, 109 (2024).
Google Scholar
Barratt, J. et al. IgA nephropathy: the lectin pathway and implications for targeted therapy. Kidney Int. 104, 254–264 (2023).
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).
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).
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).
Google Scholar
Petr, V. & Thurman, J. M. The role of complement in kidney disease. Nat. Rev. Nephrol. 19, 771–787 (2023).
Google Scholar
Meissner, M., Viehmann, S. F. & Kurts, C. DAMPening sterile inflammation of the kidney. Kidney Int. 95, 489–491 (2019).
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).
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).
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).
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).
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).
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).
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).
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).
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).
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).
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).
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).
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).
Google Scholar
Thakur, M. et al. NETs-induced thrombosis impacts on cardiovascular and chronic kidney disease. Circ. Res. 132, 933–949 (2023).
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).
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).
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).
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).
Google Scholar
Miao, N. et al. Oxidized mitochondrial DNA induces gasdermin D oligomerization in systemic lupus erythematosus. Nat. Commun. 14, 872 (2023).
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).
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).
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).
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).
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).
Google Scholar
Culemann, S. et al. Stunning of neutrophils accounts for the anti-inflammatory effects of clodronate liposomes. J. Exp. Med. 220, e20220525 (2023).
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).
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).
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).
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).
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).
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).
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).
Google Scholar
Huen, S. C. & Cantley, L. G. Macrophages in renal injury and repair. Annu. Rev. Physiol. 79, 449–469 (2017).
Google Scholar
Zhang, M. Z. et al. CSF-1 signaling mediates recovery from acute kidney injury. J. Clin. Invest. 122, 4519–4532 (2012).
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).
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).
Google Scholar
Kim, S. R. et al. Progressive cellular senescence mediates renal dysfunction in ischemic nephropathy. J. Am. Soc. Nephrol. 32, 1987–2004 (2021).
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).
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).
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).
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).
Google Scholar
Meng, X. M. et al. Inflammatory macrophages can transdifferentiate into myofibroblasts during renal fibrosis. Cell Death Dis. 7, e2495 (2016).
Google Scholar
Chung, J. Y. et al. Immunodynamics of macrophages in renal fibrosis. Integr. Med. Nephrol. Androl. 10, e00001 (2023).
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).
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).
Google Scholar
Ikezumi, Y. et al. The sialoadhesin (CD169) expressing a macrophage subset in human proliferative glomerulonephritis. Nephrol. Dial. Transpl. 20, 2704–2713 (2005).
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).
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).
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).
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).
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).
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).
Google Scholar
Chalmers, S. A. et al. Macrophage depletion ameliorates nephritis induced by pathogenic antibodies. J. Autoimmun. 57, 42–52 (2015).
Google Scholar
Meng, X. M., Nikolic-Paterson, D. J. & Lan, H. Y. Inflammatory processes in renal fibrosis. Nat. Rev. Nephrol. 10, 493–503 (2014).
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).
Google Scholar
Swenson-Fields, K. I. et al. Macrophages promote polycystic kidney disease progression. Kidney Int. 83, 855–864 (2013).
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).
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).
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).
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).
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).
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).
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).
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).
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).
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).
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).
Google Scholar
Lu, J. et al. M2c macrophages protect mice from adriamycin-induced nephropathy by upregulating CD62L in Tregs. Mediators Inflamm. 2022, 1153300 (2022).
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).
Google Scholar
Bruchfeld, A., Wendt, M. & Miller, E. J. Macrophage migration inhibitory factor in clinical kidney disease. Front. Immunol. 7, 8 (2016).
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).
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).
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).
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).
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).
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).
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).
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).
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).
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).
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).
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).
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).
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).
Google Scholar
Lan, H. Y. Macrophage-myofibroblast transition in kidney disease. Integr. Med. Nephrol. Androl. 9, 12 (2022).
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).
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).
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).
Google Scholar
Chen, J. et al. P2Y12 inhibitor clopidogrel inhibits renal fibrosis by blocking macrophage-to-myofibroblast transition. Mol. Ther. 30, 3017–3033 (2022).
Google Scholar
Kuppe, C. et al. Decoding myofibroblast origins in human kidney fibrosis. Nature 589, 281–286 (2021).
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).
Google Scholar
Tadagavadi, R. K. & Reeves, W. B. Renal dendritic cells ameliorate nephrotoxic acute kidney injury. J. Am. Soc. Nephrol. 21, 53–63 (2010).
Google Scholar
Lv, D. et al. Advances in understanding of dendritic cell in the pathogenesis of acute kidney injury. Front. Immunol. 15, 1294807 (2024).
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).
Google Scholar
Li, J. S. Y. et al. Tolerogenic dendritic cells protect against acute kidney injury. Kidney Int. 104, 492–507 (2023).
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).
Google Scholar
Jia, P. et al. Depletion of miR-21 in dendritic cells aggravates renal ischemia-reperfusion injury. FASEB J. 34, 11729–11740 (2020).
Google Scholar
Li, L. et al. Dendritic cells tolerized with adenosine A2AR agonist attenuate acute kidney injury. J Clin. Invest. 122, 3931–3942 (2012).
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).
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).
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).
Google Scholar
Arazi, A. et al. The immune cell landscape in kidneys of patients with lupus nephritis. Nat. Immunol. 20, 902–914 (2019).
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).
Google Scholar
Chen, T. et al. Conventional type 1 dendritic cells (cDC1) in human kidney diseases: clinico-pathological correlations. Front. Immunol. 12, 635212 (2021).
Google Scholar
Zheng, D. et al. Lipopolysaccharide-pretreated plasmacytoid dendritic cells ameliorate experimental chronic kidney disease. Kidney Int. 81, 892–902 (2012).
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).
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).
Google Scholar
Brahler, S. et al. Opposing roles of dendritic cell subsets in experimental GN. J. Am. Soc. Nephrol. 29, 138–154 (2018).
Google Scholar
McKenzie, A. N. J., Spits, H. & Eberl, G. Innate lymphoid cells in inflammation and immunity. Immunity 41, 366–374 (2014).
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).
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).
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).
Google Scholar
Akcay, A. et al. IL-33 exacerbates acute kidney injury. J. Am. Soc. Nephrol. 22, 2057–2067 (2011).
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).
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).
Google Scholar
Vely, F. et al. Evidence of innate lymphoid cell redundancy in humans. Nat. Immunol. 17, 1291–1299 (2016).
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).
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).
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).
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).
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).
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).
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).
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).
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).
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).
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).
Google Scholar
Zheng, G. et al. NK cells do not mediate renal injury in murine adriamycin nephropathy. Kidney Int. 69, 1159–1165 (2006).
Google Scholar
Vibhushan, S. et al. Mast cell chymase and kidney disease. Int. J. Mol. Sci. 22, 302 (2020).
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).
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).
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).
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).
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).
Google Scholar
Kim, D. H. et al. Mast cells decrease renal fibrosis in unilateral ureteral obstruction. Kidney Int. 75, 1031–1038 (2009).
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).
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).
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).
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).
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).
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).
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).
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).
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).
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).
Google Scholar
Robinson, W. H. et al. Cutting-edge approaches to B-cell depletion in autoimmune diseases. Front. Immunol. 15, 1454747 (2024).
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).
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).
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).
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).
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).
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).
Google Scholar
Wooden, B., Tarragon, B., Navarro-Torres, M. & Bomback, A. S. Complement inhibitors for kidney disease. Nephrol. Dial. Transpl. 38, ii29–ii39 (2023).
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).
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).
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).
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).
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).
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).
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).
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).
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).
Google Scholar
Gubernatorova, E. O. et al. Targeting inerleukin-6 for renoprotection. Front. Immunol. 15, 1502299 (2024).
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).
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).
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).
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).
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).
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).
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).
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).
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).
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).
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).
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).
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).
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).
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).
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).
Google Scholar
Voelker, J. et al. Anti-TGF-β1 antibody therapy in patients with diabetic nephropathy. J. Am. Soc. Nephrol. 28, 953–962 (2017).
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).
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).
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).
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).
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).
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).
Google Scholar
Li, J. et al. Role of miRNAs in macrophage-mediated kidney injury. Pediatr. Nephrol. 39, 3397–3410 (2024).
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).
Google Scholar
Johnnidis, J. B. et al. Regulation of progenitor cell proliferation and granulocyte function by microRNA-223. Nature 451, 1125–1129 (2008).
Google Scholar
Oliveira, M. C. et al. Eosinophils protect from metabolic alterations triggered by obesity. Metabolism 146, 155613 (2023).
Google Scholar
Chen, Y. et al. Basophil differentiation, heterogeneity, and functional implications. Trends Immunol. 45, 523–534 (2024).
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).
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).
Google Scholar
Palucka, K. & Banchereau, J. Cancer immunotherapy via dendritic cells. Nat. Rev. Cancer 12, 265–277 (2012).
Google Scholar
Feng, J. et al. Clonal lineage tracing reveals shared origin of conventional and plasmacytoid dendritic cells. Immunity 55, 405–422.e11 (2022).
Google Scholar
Vivier, E. et al. Innate lymphoid cells: 10 years on. Cell 174, 1054–1066 (2018).
Google Scholar
Bryceson, Y. T. et al. Functional analysis of human NK cells by flow cytometry. Methods Mol. Biol. 612, 335–352 (2010).
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).
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).
Google Scholar
Waterholter, A., Wunderlich, M. & Turner, J. E. MAIT cells in immune-mediated tissue injury and repair. Eur. J. Immunol. 53, e2350483 (2023).
Google Scholar
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