Evidence map›Paper›PMID 31275306›Full record

ArticleFrontiers in immunology2019

Protease Activated Receptor 4 as a Novel Modulator of Regulatory T Cell Function.

Qi Peng, Kulachelvy Ratnasothy, Dominic A Boardman, Jacinta Jacob, Sim Lai Tung, Daniel McCluskey, Lesley A Smyth, Robert I Lechler, Anthony Dorling, Giovanna Lombardi

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
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  7. Review
  8. Platelets differentially modulate CD4Immunologic research · 2022
    Article
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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

10 authors at 4 institutions in 1 country.

Qi PengMRC Centre for Transplantation, Guy's Hospital, King's College London, London, United Kingdom.
Kulachelvy RatnasothyMRC Centre for Transplantation, Guy's Hospital, King's College London, London, United Kingdom.
Dominic A BoardmanMRC Centre for Transplantation, Guy's Hospital, King's College London, London, United Kingdom.
Jacinta JacobMRC Centre for Transplantation, Guy's Hospital, King's College London, London, United Kingdom.
Sim Lai TungMRC Centre for Transplantation, Guy's Hospital, King's College London, London, United Kingdom.
Daniel McCluskeyMRC Centre for Transplantation, Guy's Hospital, King's College London, London, United Kingdom.
Lesley A SmythMRC Centre for Transplantation, Guy's Hospital, King's College London, London, United Kingdom.
Robert I LechlerMRC Centre for Transplantation, Guy's Hospital, King's College London, London, United Kingdom.
Anthony DorlingMRC Centre for Transplantation, Guy's Hospital, King's College London, London, United Kingdom.
Giovanna LombardiMRC Centre for Transplantation, Guy's Hospital, King's College London, London, United Kingdom.
Guy's Hospital · GBKing's College London · GBGuy's and St Thomas' NHS Foundation Trust · GBUniversity of East London · GB

Funding

British Heart Foundation RG/13/12/30395Medical Research Council G0401591Medical Research Council MR/J006742/1
6 · The paper itself

Abstract

Regulatory T cells (Tregs) are a subpopulation of T cells that maintain immunological tolerance. In inflammatory responses the function of Tregs is tightly controlled by several factors including signaling through innate receptors such as Toll like receptors and anaphylatoxin receptors allowing an effective immune response to be generated. Protease-activated receptors (PARs) are another family of innate receptors expressed on multiple cell types and involved in the pathogenesis of autoimmune disorders. Whether proteases are able to directly modulate Treg function is unknown. Here, we show using two complimentary approaches that signaling through PAR-4 influences the expression of CD25, CD62L, and CD73, the suppressive capacity, and the stability of Tregs

Indexed as

AnimalsAutoimmune DiseasesCells, CulturedForkhead Transcription FactorsImmune ToleranceMiceMice, Inbred BALB CMice, Inbred C57BLPTEN PhosphohydrolaseReceptors, ThrombinSignal TransductionT-Lymphocytes, RegulatoryForkhead Transcription Factorsprotease-activated receptor 4PTEN PhosphohydrolaseReceptors, Thrombinforkhead box protein O1 (FoxO1)immunoregulationphosphatase and tensin homolog on chromosome 10 (PTEN)PI3K/Akt signaling pathwayprotease activated receptor 4 (PAR4)regulatory T cells (Tregs)

Identifiers

PMID31275306
PMCPMC6591367
OpenAlexW2950926829

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.