Corrigendum Open Access | 10.1172/jci.insight.171762
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Published May 22, 2023 - More info
Lupus nephritis is a serious complication of systemic lupus erythematosus, mediated by IgG immune complex (IC) deposition in kidneys, with limited treatment options. Kidney macrophages are critical tissue sentinels that express IgG-binding Fcγ receptors (FcγRs), with previous studies identifying prenatally seeded resident macrophages as major IC responders. Using single-cell transcriptomic and spatial analyses in murine and human lupus nephritis, we sought to understand macrophage heterogeneity and subset-specific contributions in disease. In lupus nephritis, the cell fate trajectories of tissue-resident (TrMac) and monocyte-derived (MoMac) kidney macrophages were perturbed, with disease-associated transcriptional states indicating distinct pathogenic roles for TrMac and MoMac subsets. Lupus nephritis–associated MoMac subsets showed marked induction of FcγR response genes, avidly internalized circulating ICs, and presented IC-opsonized antigen. In contrast, lupus nephritis–associated TrMac subsets demonstrated limited IC uptake, but expressed monocyte chemoattractants, and their depletion attenuated monocyte recruitment to the kidney. TrMacs also produced B cell tissue niche factors, suggesting a role in supporting autoantibody-producing lymphoid aggregates. Extensive similarities were observed with human kidney macrophages, revealing cross-species transcriptional disruption in lupus nephritis. Overall, our study suggests a division of labor in the kidney macrophage response in lupus nephritis, with treatment implications — TrMacs orchestrate leukocyte recruitment while MoMacs take up and present IC antigen.
Nathan Richoz, Zewen K. Tuong, Kevin W. Loudon, Eduardo Patiño-Martínez, John R. Ferdinand, Jorge Romo-Tena, Anaïs Portet, Kathleen R. Bashant, Emeline Thevenon, Francesca Rucci, Thomas Hoyler, Tobias Junt, Mariana J. Kaplan, Richard M. Siegel, Menna R. Clatworthy
Original citation: JCI Insight. 2022;7(21):e159751. https://doi.org/10.1172/jci.insight.159751
Citation for this corrigendum: JCI Insight. 2023;8(10):e171762. https://doi.org/10.1172/jci.insight.171762
Jorge Romo-Tena’s name was inadvertently omitted from the author list and Author contributions section. The correct author and affiliations lists and sentence from the Author contributions section are below. The HTML and PDF versions have been updated online.
Nathan Richoz,1,2,3 Zewen K. Tuong,1,2,4 Kevin W. Loudon,1,2 Eduardo Patiño-Martínez,3 John R. Ferdinand,1,2 Anaïs Portet,1,2 Jorge Romo-Tena,3 Kathleen R. Bashant,3 Emeline Thevenon,5 Francesca Rucci,5 Thomas Hoyler,5 Tobias Junt,5 Mariana J. Kaplan,3 Richard M. Siegel,3,5 Menna R. Clatworthy1,2,4
1Molecular Immunity Unit, University of Cambridge Department of Medicine, Medical Research Council Laboratory of Molecular Biology, Cambridge, United Kingdom. 2Cambridge Institute of Therapeutic Immunology and Infectious Diseases, Department of Medicine, University of Cambridge School of Clinical Medicine, Cambridge, United Kingdom. 3National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, USA. 4Cellular Genetics Programme, Wellcome Sanger Institute, Hinxton, United Kingdom. 5Novartis Institutes for BioMedical Research, Basel, Switzerland.
Conducting experiments was contributed by NR, KWL, EPM, JRF, AP, and JRT.
See the related article at Distinct pathogenic roles for resident and monocyte-derived macrophages in lupus nephritis.