Evidence map›Paper›PMID 32868399›Full record

ArticleJournal of the American Society of Nephrology : JASN2020

Live Imaging of Monocyte Subsets in Immune Complex-Mediated Glomerulonephritis Reveals Distinct Phenotypes and Effector Functions.

Tabitha Turner-Stokes, Ana Garcia Diaz, Damilola Pinheiro, Maria Prendecki, Stephen P McAdoo, Candice Roufosse, H Terence Cook, Charles D Pusey, Kevin J Woollard

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 13% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. The Src-Family Kinases Hck, Fgr and Lyn Drive Immune Complex-Mediated Glomerulonephritis Through the Syk Tyrosine Kinase.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  4. Kidney Disease as a Driver of Immunosenescence: Mechanisms and Potential Interventions.Journal of the American Society of Nephrology : JASN · 2026
    Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Monocytes and Macrophages in Kidney Disease and Homeostasis.International journal of molecular sciences · 2024
    Review
  10. Genetic and Immunohistochemistry Tools to Visualize Rat Macrophages In Situ.Methods in molecular biology (Clifton, N.J.) · 2024
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
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

9 authors at 1 institution in 1 country.

Tabitha Turner-StokesCentre for Inflammatory Disease, Imperial College London, London, UK.
Ana Garcia DiazCentre for Inflammatory Disease, Imperial College London, London, UK.
Damilola PinheiroCentre for Inflammatory Disease, Imperial College London, London, UK.
Maria PrendeckiCentre for Inflammatory Disease, Imperial College London, London, UK.
Stephen P McAdooCentre for Inflammatory Disease, Imperial College London, London, UK.
Candice RoufosseCentre for Inflammatory Disease, Imperial College London, London, UK.
H Terence CookCentre for Inflammatory Disease, Imperial College London, London, UK.
Charles D PuseyCentre for Inflammatory Disease, Imperial College London, London, UK.
Kevin J WoollardCentre for Inflammatory Disease, Imperial College London, London, UK k.woollard@imperial.ac.uk.ORCID 0000-0002-9839-5463
Imperial College London · GB

Funding

British Heart Foundation PG/18/41/33813Medical Research Council MR/M003159/1
6 · The paper itself

Abstract

backgroundImmune complexes within glomerular capillary walls cause crescentic GN (CrGN). Monocytes and macrophages are important in mediating CrGN, but little work has been done to phenotype the subpopulations involved and determine their respective contributions to glomerular inflammation.

methodsLive glomerular imaging using confocal microscopy monitored intravascular monocyte subset behavior during nephrotoxic nephritis (NTN) in a novel WKY-hCD68-GFP monocyte/macrophage reporter rat strain. Flow cytometry and qPCR further analyzed

resultsNon-classical monocytes surveyed the glomerular endothelium

conclusionsMonocyte subsets with distinct phenotypes and effector functions may be important in driving inflammation in experimental CrGN resulting from immune complexes formed within the glomerular capillary wall. LFA-1-dependent endothelial surveillance by non-classical monocytes may detect immune complexes through CD16, orchestrating the inflammatory response through intravascular retention of classical monocytes, which results in glomerular damage and proteinuria.

Indexed as

AnimalsAntigens, CDAntigens, Differentiation, MyelomonocyticCapillariesCD68 MoleculeCell MovementEndotheliumFlow CytometryGlomerulonephritisIntravital MicroscopyKidney GlomerulusMaleMicroscopy, ConfocalMonocytesPhenotypeRatsAntigens, CDAntigens, Differentiation, MyelomonocyticCD68 MoleculeCD68 protein, ratFcgr2a protein, ratReceptors, IgGglomerulonephritisimmune complexesimmunologymacrophages

Identifiers

PMID32868399
PMCPMC7608972
OpenAlexW3082919424

What OpenQuestion holds

Textmetadata
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.