Evidence map›Paper›PMID 31793912›Full record

ArticleThe Journal of clinical investigation2020

GPR101 mediates the pro-resolving actions of RvD5n-3 DPA in arthritis and infections.

Magdalena B Flak, Duco S Koenis, Agua Sobrino, James Smith, Kimberly Pistorius, Francesco Palmas, Jesmond Dalli

Open access · hybridAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

62 citing papers in PubMed, 95 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. 10-epi-Protectin DX and Resolvin D5International journal of molecular sciences · 2026
    Article
  5. Article
  6. Article
  7. Review
  8. Beyond Killing: The Overlooked Contribution of Neutrophils to Tissue Repair.International journal of molecular sciences · 2025
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
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  19. Article
  20. Review

2 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 1 country.

Magdalena B FlakWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, and.
Duco S KoenisWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, and.
Agua SobrinoWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, and.
James SmithWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, and.
Kimberly PistoriusWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, and.
Francesco PalmasWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, and.
Jesmond DalliWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, and.
William Harvey Research Institute · GBQueen Mary University of London · GB

Funding

European Research Council 677542Wellcome Trust
6 · The paper itself

Abstract

N-3 docosapentaenoic acid-derived resolvin D5 (RvD5n-3 DPA) is diurnally regulated in peripheral blood and exerts tissue-protective actions during inflammatory arthritis. Here, using an orphan GPCR screening approach coupled with functional readouts, we investigated the receptor(s) involved in mediating the leukocyte-directed actions of RvD5n-3 DPA and identified GPR101 as the top candidate. RvD5n-3 DPA bound to GPR101 with high selectivity and stereospecificity, as demonstrated by a calculated KD of approximately 6.9 nM. In macrophages, GPR101 knockdown limited the ability of RvD5n-3 DPA to upregulate cyclic adenosine monophosphate, phagocytosis of bacteria, and efferocytosis. Inhibition of this receptor in mouse and human leukocytes abrogated the pro-resolving actions of RvD5n-3 DPA, including the regulation of bacterial phagocytosis in neutrophils. Knockdown of the receptor in vivo reversed the protective actions of RvD5n-3 DPA in limiting joint and gut inflammation during inflammatory arthritis. Administration of RvD5n-3 DPA during E. coli-initiated inflammation regulated neutrophil trafficking to the site of inflammation, increased bacterial phagocytosis by neutrophils and macrophages, and accelerated the resolution of infectious inflammation. These in vivo protective actions of RvD5n-3 DPA were limited when Gpr101 was knocked down. Together, our findings demonstrate a fundamental role for GPR101 in mediating the leukocyte-directed actions of RvD5n-3 DPA.

Indexed as

AnimalsArthritisCHO CellsCricetulusDocosahexaenoic AcidsEscherichia coliEscherichia coli InfectionsGene Knockdown TechniquesHumansMacrophagesMaleMiceNeutrophilsPhagocytosisReceptors, G-Protein-CoupledDocosahexaenoic AcidsGPR101 protein, humanReceptors, G-Protein-Coupledresolvin D5ArthritisBacterial infectionsG-protein coupled receptorsInfectious diseaseInflammation

Identifiers

PMID31793912
PMCPMC6934227
OpenAlexW2994572080

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.