Evidence map›Paper›PMID 30507064›Full record

ReviewArthritis & rheumatology (Hoboken, N.J.)2019

The Contribution of PTPN22 to Rheumatic Disease.

Tomas Mustelin, Nunzio Bottini, Stephanie M Stanford

Abstract readReview
In one paragraph

Review in Arthritis & rheumatology (Hoboken, N.J.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 12% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Pooled it
  2. Review
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  6. Review
  7. Article
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  14. Article
  15. OT-I TCR Transgenic Mice to Study the Role of PTPN22 in Anti-cancer Immunity.Methods in molecular biology (Clifton, N.J.) · 2024
    Article
  16. Review
  17. Review
  18. Analysis ofDiagnostics (Basel, Switzerland) · 2023
    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

3 authors at 2 institutions in 1 country.

Tomas MustelinUniversity of Washington, Seattle.
Nunzio BottiniUniversity of California at San Diego, La Jolla.
Stephanie M StanfordUniversity of California at San Diego, La Jolla.
University of California, San Diego · USUniversity of Washington · US

Funding

PTPN22 AND AUTOIMMUNITYR01AI070544 · NIAID · UNIVERSITY OF SOUTHERN CALIFORNIA · PI BOTTINI, NUNZIO · 2008 to 2019
$4.0M
Role of PTPRS in Rheumatoid ArtiritisR01AR066053 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BOTTINI, NUNZIO · 2014 to 2025
$4.0M
Negative regulation of TCR-associated PTKsR01AI053585 · NIAID · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI RICKERT, ROBERT C · 2003 to 2007
$2.1M
Role of protein citrullination in rheumatoid arthritisR01AR074939 · NIAMS · UNIVERSITY OF WASHINGTON · PI MUSTELIN, TOMAS M · 2020 to 2024
$1.9M
NIAID NIH HHS R01 AI053585NIAID NIH HHS R01 AI070544NIAMS NIH HHS R01 AR066053NIAMS NIH HHS R01 AR074939
6 · The paper itself

Abstract

One of the unresolved questions in modern medicine is why certain individuals develop a disorder such as rheumatoid arthritis (RA) or lupus, while others do not. Contemporary science indicates that genetics is partly responsible for disease development, while environmental and stochastic factors also play a role. Among the many genes that increase the risk of autoimmune conditions, the risk allele encoding the W620 variant of protein tyrosine phosphatase N22 (PTPN22) is shared between multiple rheumatic diseases, suggesting that it plays a fundamental role in the development of immune dysfunction. Herein, we discuss how the presence of the PTPN22 risk allele may shape the signs and symptoms of these diseases. Besides the emerging clarity regarding how PTPN22 tunes T and B cell antigen receptor signaling, we discuss recent discoveries of important functions of PTPN22 in myeloid cell lineages. Taken together, these new insights reveal important clues to the molecular mechanisms of prevalent diseases like RA and lupus and may open new avenues for the development of personalized therapies that spare the normal function of the immune system.

Indexed as

AllelesGenetic Predisposition to DiseaseHumansProtein Tyrosine Phosphatase, Non-Receptor Type 22Rheumatic DiseasesRisk FactorsProtein Tyrosine Phosphatase, Non-Receptor Type 22PTPN22 protein, human

Identifiers

PMID30507064
PMCPMC6438733
OpenAlexW2903018958

What OpenQuestion holds

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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.