Evidence map›Paper›PMID 36345939›Full record

ArticleJCI insight2022

Distinct pathogenic roles for resident and monocyte-derived macrophages in lupus nephritis.

Nathan Richoz, Zewen K Tuong, Kevin W Loudon, Eduardo Patiño-Martínez, John R Ferdinand, Anaïs Portet, Kathleen R Bashant, Emeline Thevenon, Francesca Rucci, Thomas Hoyler and 4 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
9.4field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

49 citing papers in PubMed, 56 citations in OpenAlex.

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  17. Lupus nephritis.Nature reviews. Disease primers · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 3 institutions in 4 countries.

Nathan RichozMolecular Immunity Unit, University of Cambridge Department of Medicine, Medical Research Council Laboratory of Molecular Biology, Cambridge, United Kingdom.
Zewen K TuongMolecular Immunity Unit, University of Cambridge Department of Medicine, Medical Research Council Laboratory of Molecular Biology, Cambridge, United Kingdom.
Kevin W LoudonMolecular Immunity Unit, University of Cambridge Department of Medicine, Medical Research Council Laboratory of Molecular Biology, Cambridge, United Kingdom.
Eduardo Patiño-MartínezNational Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, USA.
John R FerdinandMolecular Immunity Unit, University of Cambridge Department of Medicine, Medical Research Council Laboratory of Molecular Biology, Cambridge, United Kingdom.
Anaïs PortetMolecular Immunity Unit, University of Cambridge Department of Medicine, Medical Research Council Laboratory of Molecular Biology, Cambridge, United Kingdom.
Kathleen R BashantNational Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Emeline ThevenonNovartis Institutes for BioMedical Research, Basel, Switzerland.
Francesca RucciNovartis Institutes for BioMedical Research, Basel, Switzerland.
Thomas HoylerNovartis Institutes for BioMedical Research, Basel, Switzerland.
Tobias JuntNovartis Institutes for BioMedical Research, Basel, Switzerland.
Mariana J KaplanNational Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Richard M SiegelNational Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Menna R ClatworthyMolecular Immunity Unit, University of Cambridge Department of Medicine, Medical Research Council Laboratory of Molecular Biology, Cambridge, United Kingdom.
MRC Laboratory of Molecular Biology · GBNovartis (Switzerland) · CHNational Institutes of Health · US

Funding

Systemic AutoimmunityZIAAR041199 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI KAPLAN, MARIANA · 2014 to 2025
$32.5M
TNF-receptors and programmed cell death in regulation of autoimmunityZIAAR041133 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI SIEGEL, RICHARD M · 2009 to 2019
$9.3M
TNF-Family receptors in immune homeostasis and diseaseZ01AR041133 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI SIEGEL, RICHARD M · 2002 to 2008
$2.6M
Department of HealthIntramural NIH HHS Z01 AR041133Intramural NIH HHS ZIA AR041133Intramural NIH HHS ZIA AR041199Medical Research Council MR/N024907/1Medical Research Council MR/S035842/1Versus Arthritis 21777Wellcome TrustWellcome Trust 106809/Z/15/ZWellcome Trust 220268/Z/20/Z
6 · The paper itself

Abstract

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.

Indexed as

Lupus Erythematosus, SystemicLupus NephritisAnimalsHumansImmunoglobulin GMacrophagesMiceMonocytesReceptors, IgGImmunoglobulin GReceptors, IgGAutoimmunityImmunologyLupusMacrophages

Identifiers

PMID36345939
PMCPMC9675473
OpenAlexW4308391437

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.