Evidence map›Paper›PMID 27807193›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2016

PTPN22 Is a Critical Regulator of Fcγ Receptor-Mediated Neutrophil Activation.

Sonja Vermeren, Katherine Miles, Julia Y Chu, Donald Salter, Rose Zamoyska, Mohini Gray

Open access · hybridAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

28 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Protein phosphatases in systemic autoimmunity.Immunometabolism (Cobham, Surrey) · 2025
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  6. Review
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  9. Review
  10. Overexpression of theJournal of immunology (Baltimore, Md. : 1950) · 2021
    Article
  11. A Darwinian View of Behçet's Disease.Rheumatology and immunology research · 2021
    Review
  12. De-coding genetic risk variants in type 1 diabetes.Immunology and cell biology · 2021
    Review
  13. Article
  14. Influence ofFrontiers in immunology · 2021
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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

6 authors at 3 institutions in 1 country.

Sonja VermerenMedical Research Council/University of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, Edinburgh EH16 4TJ, United Kingdom; Sonja.Vermeren@ed.ac.uk Mohini.Gray@ed.ac.uk.ORCID 0000-0002-8460-0884
Katherine MilesMedical Research Council/University of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, Edinburgh EH16 4TJ, United Kingdom.
Julia Y ChuMedical Research Council/University of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, Edinburgh EH16 4TJ, United Kingdom.
Donald SalterInstitute for Genetics and Molecular Medicine, Edinburgh EH4 2XU, United Kingdom; and.ORCID 0000-0002-4451-4375
Rose ZamoyskaInstitute of Immunology and Infection Research, Ashworth Laboratories, University of Edinburgh, Edinburgh EH9 3FL, United Kingdom.ORCID 0000-0001-9816-2638
Mohini GrayMedical Research Council/University of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, Edinburgh EH16 4TJ, United Kingdom; Sonja.Vermeren@ed.ac.uk Mohini.Gray@ed.ac.uk.ORCID 0000-0002-7622-214X
Queen's Medical Centre · GBCentre for Immunity, Infection and Evolution · GBInstitute of Genetics and Cancer · GB

Funding

Arthritis Research UK 20035Cancer Research UK 20035Medical Research Council G0700740Medical Research Council MR/J009555/1Wellcome Trust
6 · The paper itself

Abstract

Neutrophils act as a first line of defense against bacterial and fungal infections, but they are also important effectors of acute and chronic inflammation. Genome-wide association studies have established that the gene encoding the protein tyrosine phosphatase nonreceptor 22 (PTPN22) makes an important contribution to susceptibility to autoimmune disease, notably rheumatoid arthritis. Although PTPN22 is most highly expressed in neutrophils, its function in these cells remains poorly characterized. We show in this article that neutrophil effector functions, including adhesion, production of reactive oxygen species, and degranulation induced by immobilized immune complexes, were reduced in Ptpn22

Indexed as

AnimalsAntigen-Antibody ComplexArthritis, ExperimentalArthritis, RheumatoidCell AdhesionCell DegranulationGenetic Predisposition to DiseaseHumansMiceMice, Inbred C57BLMice, KnockoutNeutrophil ActivationNeutrophilsPhosphorylationPolymorphism, GeneticProtein Tyrosine Phosphatase, Non-Receptor Type 22Antigen-Antibody Complexlyn protein-tyrosine kinaseProtein Tyrosine Phosphatase, Non-Receptor Type 22Ptpn22 protein, mouseReactive Oxygen SpeciesReceptors, IgGsrc-Family KinasesSyk KinaseSyk protein, mouse

Identifiers

PMID27807193
PMCPMC5136470
OpenAlexW2548330268

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.