Evidence map›Paper›PMID 36928841›Full record

ReviewImmunological reviews2023

GPR35 and mediators from platelets and mast cells in neutrophil migration and inflammation.

Marco De Giovanni, Hongwen Chen, Xiaochun Li, Jason G Cyster

Open access · greenAbstract readReview
In one paragraph

Review in Immunological reviews, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
6.9field-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

18 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. Platelet-mast cell dialogue in innate immune response and inflammation.American journal of physiology. Lung cellular and molecular physiology · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. 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

4 authors at 2 institutions in 1 country.

Marco De GiovanniDepartment of Microbiology and Immunology, Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, California, USA.
Hongwen ChenDepartments of Molecular Genetics and Biophysics, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Xiaochun LiDepartments of Molecular Genetics and Biophysics, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Jason G CysterDepartment of Microbiology and Immunology, Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, California, USA.ORCID 0000-0002-4735-9745
Howard Hughes Medical Institute · USThe University of Texas Southwestern Medical Center · US

Funding

Chemokines and Lymphoid Tissue Organization and FunctionR01AI045073 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CYSTER, JASON G · 1999 to 2023
$7.6M
Chemokines and Lymphoid Tissue Organization and FunctionR37AI045073 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Jason G Cyster · 2024 to 2026
$1.7M
GPR35 function in the immune systemR21AI163036 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CYSTER, JASON G · 2021 to 2022
$444k
Howard Hughes Medical InstituteNIAID NIH HHS R01 AI045073NIAID NIH HHS R21 AI163036NIAID NIH HHS R37 AI045073
6 · The paper itself

Abstract

Neutrophil recruitment from circulation to sites of inflammation is guided by multiple chemoattractant cues emanating from tissue cells, immune cells, and platelets. Here, we focus on the function of one G-protein coupled receptor, GPR35, in neutrophil recruitment. GPR35 has been challenging to study due the description of multiple ligands and G-protein couplings. Recently, we found that GPR35-expressing hematopoietic cells respond to the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA). We discuss distinct response profiles of GPR35 to 5-HIAA compared to other ligands. To place the functions of 5-HIAA in context, we summarize the actions of serotonin in vascular biology and leukocyte recruitment. Important sources of serotonin and 5-HIAA are platelets and mast cells. We discuss the dynamics of cell migration into inflamed tissues and how multiple platelet and mast cell-derived mediators, including 5-HIAA, cooperate to promote neutrophil recruitment. Additional actions of GPR35 in tissue physiology are reviewed. Finally, we discuss how clinically approved drugs that modulate serotonin uptake and metabolism may influence 5-HIAA-GPR35 function, and we speculate about broader influences of the GPR35 ligand-receptor system in immunity and disease.

Indexed as

Mast CellsNeutrophilsBlood PlateletsCell MovementHumansHydroxyindoleacetic AcidInflammationLigandsNeutrophil InfiltrationReceptors, G-Protein-CoupledSerotoninGPR35 protein, humanHydroxyindoleacetic AcidLigandsReceptors, G-Protein-CoupledSerotoninchemotaxisGPCRslipid mediatorsmast cellsneutrophilsplatelets

Identifiers

PMID36928841
PMCPMC10504419
OpenAlexW4327590763

What OpenQuestion holds

Textmetadata
LicenceTDM
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.