Evidence map›Paper›PMID 35404389›Full record

ArticleThe Journal of experimental medicine2022

Monocytes transition to macrophages within the inflamed vasculature via monocyte CCR2 and endothelial TNFR2.

Vijayashree Mysore, Suhail Tahir, Kazuhiro Furuhashi, Jatin Arora, Florencia Rosetti, Xavier Cullere, Pascal Yazbeck, Miroslav Sekulic, Madeleine E Lemieux, Soumya Raychaudhuri and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

47 citing papers in PubMed, 74 citations in OpenAlex.

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  13. Xcr1eLife · 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

12 authors at 4 institutions in 3 countries.

Vijayashree Mysore *Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
Suhail Tahir *Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.ORCID 0000-0002-0375-8701
Kazuhiro Furuhashi *Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.ORCID 0000-0003-2476-688X
Jatin Arora *Center for Data Sciences, Brigham and Women's Hospital, Boston, MA.
Florencia Rosetti *Department of Immunology and Rheumatology, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico.ORCID 0000-0001-7270-4515
Xavier CullereDepartment of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.ORCID 0000-0001-6983-4714
Pascal YazbeckDepartment of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
Miroslav SekulicDepartment of Pathology and Cell Biology, Columbia University Irving Medical Center, New York, NY.ORCID 0000-0002-7938-1816
Madeleine E LemieuxBioinfo, Plantagenet, Ontario, Canada.ORCID 0000-0001-6355-8691
Soumya Raychaudhuri *Center for Data Sciences, Brigham and Women's Hospital, Boston, MA.ORCID 0000-0002-1901-8265
Bruce H Horwitz *Department of Pediatrics, Boston Children's Hospital and Harvard Medical School, Boston, MA.ORCID 0000-0002-8123-8728
Tanya N MayadasDepartment of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.ORCID 0000-0002-3604-4457
Brigham and Women's Hospital · USBoston Children's Hospital · USColumbia University Irving Medical Center · USInstituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán · MX

Funding

Regulators of Immune Complex Mediated Neutrophil Recruitment and Tissue InjuryR01HL065095 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI MAYADAS, TANYA N · 1999 to 2025
$11.9M
TNFR2 Regulation of Leukocyte Recruitment in GlomerulonephritisR01DK099507 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI MAYADAS, TANYA N · 2014 to 2018
$2.1M
NHLBI NIH HHS R01 HL065095NIDDK NIH HHS R01 DK099507
6 · The paper itself

Abstract

Monocytes undergo phenotypic and functional changes in response to inflammatory cues, but the molecular signals that drive different monocyte states remain largely undefined. We show that monocytes acquire macrophage markers upon glomerulonephritis and may be derived from CCR2+CX3CR1+ double-positive monocytes, which are preferentially recruited, dwell within glomerular capillaries, and acquire proinflammatory characteristics in the nephritic kidney. Mechanistically, the transition to immature macrophages begins within the vasculature and relies on CCR2 in circulating cells and TNFR2 in parenchymal cells, findings that are recapitulated in vitro with monocytes cocultured with TNF-TNFR2-activated endothelial cells generating CCR2 ligands. Single-cell RNA sequencing of cocultures defines a CCR2-dependent monocyte differentiation path associated with the acquisition of immune effector functions and generation of CCR2 ligands. Immature macrophages are detected in the urine of lupus nephritis patients, and their frequency correlates with clinical disease. In conclusion, CCR2-dependent functional specialization of monocytes into macrophages begins within the TNF-TNFR2-activated vasculature and may establish a CCR2-based autocrine, feed-forward loop that amplifies renal inflammation.

Indexed as

Endothelial CellsMonocytesReceptors, CCR2Receptors, Tumor Necrosis Factor, Type IIHumansLigandsMacrophagesCCR2 protein, humanLigandsReceptors, CCR2Receptors, Tumor Necrosis Factor, Type IITNFRSF1B protein, human

Identifiers

PMID35404389
PMCPMC9006314
OpenAlexW4223580167

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

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.