Evidence map›Paper›PMID 24905474›Full record

ArticleClinical and experimental immunology2014

The protein tyrosine phosphatase PTPN22 controls forkhead box protein 3 T regulatory cell induction but is dispensable for T helper type 1 cell polarization.

G Fousteri, T Jofra, I Debernardis, S M Stanford, A Laurenzi, N Bottini, M Battaglia

Open access · greenAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

17 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. Development and function of FOXP3+ regulators of immune responses.Clinical and experimental immunology · 2023
    Article
  4. Genetic Polymorphism ofMedicina (Kaunas, Lithuania) · 2022
    Review
  5. Article
  6. Overexpression of theJournal of immunology (Baltimore, Md. : 1950) · 2021
    Article
  7. Influence ofFrontiers in immunology · 2021
    Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Genetics of immune-mediated inflammatory diseases.Clinical and experimental immunology · 2018
    Review
  15. Review
  16. Article
  17. 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

7 authors at 4 institutions in 2 countries.

G FousteriDiabetes Research Institute (DRI), IRCCS San Raffaele Scientific Institute, Milan, Italy.
T Jofra
I Debernardis
S M Stanford
A Laurenzi
N Bottini
M Battaglia
Istituti di Ricovero e Cura a Carattere Scientifico · ITLa Jolla Institute for Immunology · USIRCCS Ospedale San Raffaele · ITIstituto di Ricovero e Cura a Carattere Scientifico San Raffaele

Funding

PTPN22 AND AUTOIMMUNITYR01AI070544 · NIAID · UNIVERSITY OF SOUTHERN CALIFORNIA · PI BOTTINI, NUNZIO · 2008 to 2019
$4.0M
NIAID NIH HHS R01 AI070544NIAID NIH HHS R01AI070544
6 · The paper itself

Abstract

Protein tyrosine phosphatases (PTPs) regulate T cell receptor (TCR) signalling and thus have a role in T cell differentiation. Here we tested whether the autoimmune predisposing gene PTPN22 encoding for a PTP that inhibits TCR signalling affects the generation of forkhead box protein 3 (FoxP3)(+) T regulatory (Treg ) cells and T helper type 1 (Th1) cells. Murine CD4(+) T cells isolated from Ptpn22 knock-out (Ptpn22(KO) ) mice cultured in Treg cell polarizing conditions showed increased sensitivity to TCR activation compared to wild-type (WT) cells, and subsequently reduced FoxP3 expression at optimal-to-high levels of activation. However, at lower levels of TCR activation, Ptpn22(KO) CD4(+) T cells showed enhanced expression of FoxP3. Similar experiments in humans revealed that at optimal levels of TCR activation PTPN22 knock-down by specific oligonucleotides compromises the differentiation of naive CD4(+) T cells into Treg cells. Notably, in vivo Treg cell conversion experiments in mice showed delayed kinetic but overall increased frequency and number of Treg cells in the absence of Ptpn22. In contrast, the in vitro and in vivo generation of Th1 cells was comparable between WT and Ptpn22(KO) mice, thus suggesting PTPN22 as a FoxP3-specific regulating factor. Together, these results propose PTPN22 as a key factor in setting the proper threshold for FoxP3(+) Treg cell differentiation.

Indexed as

AnimalsCD4-Positive T-LymphocytesCell DifferentiationForkhead Transcription FactorsHumansMiceMice, Inbred C57BLMice, KnockoutProtein Tyrosine Phosphatase, Non-Receptor Type 22Receptors, Antigen, T-CellTh1 CellsT-Lymphocytes, RegulatoryForkhead Transcription FactorsProtein Tyrosine Phosphatase, Non-Receptor Type 22Receptors, Antigen, T-CellFoxP3+ Treg cellsPTPN22Th1 cells

Identifiers

PMID24905474
PMCPMC4360206
OpenAlexW1485475535

What OpenQuestion holds

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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.