Evidence map›Paper›PMID 25108421›Full record

ArticleNature immunology2014

The tyrosine phosphatase PTPN22 discriminates weak self peptides from strong agonist TCR signals.

Robert J Salmond, Rebecca J Brownlie, Vicky L Morrison, Rose Zamoyska

Open access · greenAbstract read
In one paragraph

Article in Nature immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed, 1 pooled it
5.5field-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

77 citing papers in PubMed, 1 synthesis or guideline pooled it, 104 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. OT-I TCR Transgenic Mice to Study the Role of PTPN22 in Anti-cancer Immunity.Methods in molecular biology (Clifton, N.J.) · 2024
    Article
  8. Review
  9. Article
  10. Review
  11. eLife · 2023
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. STAT1 maintains naïve CD8Science advances · 2021
    Article
  18. Overexpression of theJournal of immunology (Baltimore, Md. : 1950) · 2021
    Article
  19. Review
  20. Article

17 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

4 authors at 1 institution in 1 country.

Robert J Salmond *Institute of Immunology and Infection Research, Centre for Immunity, Infection and Evolution, Ashworth Laboratories, The King's Buildings, University of Edinburgh, West Mains Road, Edinburgh, EH9 3JT, UK.
Rebecca J Brownlie *Institute of Immunology and Infection Research, Centre for Immunity, Infection and Evolution, Ashworth Laboratories, The King's Buildings, University of Edinburgh, West Mains Road, Edinburgh, EH9 3JT, UK.
Vicky L MorrisonMedical Research Institute, Ninewells Hospital and Medical School, University of Dundee, Dundee, DD1 9SY, UK.
Rose ZamoyskaInstitute of Immunology and Infection Research, Centre for Immunity, Infection and Evolution, Ashworth Laboratories, The King's Buildings, University of Edinburgh, West Mains Road, Edinburgh, EH9 3JT, UK.
University of Dundee · GB

Funding

Biotechnology and Biological Sciences Research Council 801148Wellcome Trust 095831Wellcome Trust 096669
6 · The paper itself

Abstract

T cells must be tolerant of self antigens to avoid autoimmunity but responsive to foreign antigens to provide protection against infection. We found that in both naive T cells and effector T cells, the tyrosine phosphatase PTPN22 limited signaling via the T cell antigen receptor (TCR) by weak agonists and self antigens while not impeding responses to strong agonist antigens. T cells lacking PTPN22 showed enhanced formation of conjugates with antigen-presenting cells pulsed with weak peptides, which led to activation of the T cells and their production of inflammatory cytokines. This effect was exacerbated under conditions of lymphopenia, with the formation of potent memory T cells in the absence of PTPN22. Our data address how loss-of-function PTPN22 alleles can lead to the population expansion of effector and/or memory T cells and a predisposition to human autoimmunity.

Indexed as

AllelesAnimalsAntigen-Presenting CellsAutoimmunityLymphocyte ActivationMiceProtein Tyrosine Phosphatase, Non-Receptor Type 22Receptors, Antigen, T-CellSignal TransductionT-LymphocytesProtein Tyrosine Phosphatase, Non-Receptor Type 22Ptpn22 protein, mouseReceptors, Antigen, T-Cell

Identifiers

PMID25108421
PMCPMC4148831
OpenAlexW1970617519

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.