Evidence map›Paper›PMID 33811066›Full record

ArticleScience advances2021

Agonist anti-ChemR23 mAb reduces tissue neutrophil accumulation and triggers chronic inflammation resolution.

C Trilleaud, V Gauttier, K Biteau, I Girault, L Belarif, C Mary, S Pengam, G Teppaz, V Thepenier, R Danger and 12 more

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
7.7field-weighted citation impact, top 2% 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

51 citing papers in PubMed, 71 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review
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

22 authors at 5 institutions in 1 country.

C TrilleaudOSE Immunotherapeutics, Nantes, France.ORCID 0000-0002-6018-8178
V GauttierOSE Immunotherapeutics, Nantes, France.ORCID 0000-0002-4297-0449
K BiteauOSE Immunotherapeutics, Nantes, France.
I GiraultOSE Immunotherapeutics, Nantes, France.
L BelarifOSE Immunotherapeutics, Nantes, France.
C MaryOSE Immunotherapeutics, Nantes, France.
S PengamOSE Immunotherapeutics, Nantes, France.
G TeppazOSE Immunotherapeutics, Nantes, France.
V ThepenierOSE Immunotherapeutics, Nantes, France.
R DangerUniversité de Nantes.ORCID 0000-0002-5058-795X
G Robert-SiegwaldInovarion, Paris, France.ORCID 0000-0001-7097-4378
M NéelUniversité de Nantes.
S BruneauUniversité de Nantes.ORCID 0000-0002-1552-0725
A GlémainUniversité de Nantes.
A NéelUniversité de Nantes.
A PouponMabSillico, Nouzilly, France.ORCID 0000-0003-0617-0935
J F MosnierUniversité de Nantes.
G ChêneAmbiotis, Canal Biotech 2, Toulouse, France.
M DubourdeauAmbiotis, Canal Biotech 2, Toulouse, France.ORCID 0000-0003-3653-3768
G BlanchoUniversité de Nantes.ORCID 0000-0003-0356-5069
B VanhoveOSE Immunotherapeutics, Nantes, France.ORCID 0000-0002-2872-8648
N PoirierOSE Immunotherapeutics, Nantes, France. nicolas.poirier@ose-immuno.com.ORCID 0000-0003-2335-9385
OSE Immunotherapeutics (France) · FRInserm · FRInstitut de Transplantation Urologie en Nephrologie · FRParis Biotech Santé · FRSyndicat des Sélectionneurs Avicoles et Aquacoles Français · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Resolution of inflammation is elicited by proresolving lipids, which activate GPCRs to induce neutrophil apoptosis, reduce neutrophil tissue recruitment, and promote macrophage efferocytosis. Transcriptional analyses in up to 300 patients with Inflammatory Bowel Disease (IBD) identified potential therapeutic targets mediating chronic inflammation. We found that ChemR23, a GPCR targeted by resolvin E1, is overexpressed in inflamed colon tissues of severe IBD patients unresponsive to anti-TNFα or anti-α4β7 therapies and associated with significant mucosal neutrophil accumulation. We also identified an anti-ChemR23 agonist antibody that induces receptor signaling, promotes macrophage efferocytosis, and reduces neutrophil apoptosis at the site of inflammation. This ChemR23 mAb accelerated acute inflammation resolution and triggered resolution in ongoing chronic colitis models, with a significant decrease in tissue lesions, fibrosis and inflammation-driven tumors. Our findings suggest that failure of current IBD therapies may be associated with neutrophil infiltration and that ChemR23 is a promising therapeutic target for chronic inflammation.

Indexed as

Inflammatory Bowel DiseasesNeutrophilsAnimalsHumansInflammationMiceMice, Inbred C57BLReceptors, ChemokineReceptors, Chemokine

Identifiers

PMID33811066
PMCPMC11057782
OpenAlexW3149896748

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.