Evidence map›Paper›PMID 22611241›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

Pten loss in CD4 T cells enhances their helper function but does not lead to autoimmunity or lymphoma.

Dalya R Soond, Fabien Garçon, Daniel T Patton, Julia Rolf, Martin Turner, Cheryl Scudamore, Oliver A Garden, Klaus Okkenhaug

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

31 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. PTEN in Immunity.Current topics in microbiology and immunology · 2022
    Article
  7. Review
  8. The Effect ofJournal of oncology · 2021
    Article
  9. PI3K in T Cell Adhesion and Trafficking.Frontiers in immunology · 2021
    Review
  10. Review
  11. ZebrafishVaccines · 2020
    Article
  12. The Role of PTEN in Innate and Adaptive Immunity.Cold Spring Harbor perspectives in medicine · 2019
    Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. PI3Kδ and primary immunodeficiencies.Nature reviews. Immunology · 2016
    Review
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

8 authors at 2 institutions in 1 country.

Dalya R SoondLaboratory of Lymphocyte Signalling and Development, Babraham Institute, Cambridge CB22 3AT, United Kingdom.
Fabien Garçon
Daniel T Patton
Julia Rolf
Martin Turner
Cheryl Scudamore
Oliver A Garden
Klaus Okkenhaug
Babraham Institute · GBRoyal Veterinary College · GB

Funding

Biotechnology and Biological Sciences Research Council BB/C509890/1Biotechnology and Biological Sciences Research Council BB/E009867/1Biotechnology and Biological Sciences Research Council BB/E011659/1Biotechnology and Biological Sciences Research Council BB/E021638/1Biotechnology and Biological Sciences Research Council BB/F015461/1Biotechnology and Biological Sciences Research Council BBF0154611Biotechnology and Biological Sciences Research Council BBS/E/B/0000C207Biotechnology and Biological Sciences Research Council BBS/E/B/0000C236Biotechnology and Biological Sciences Research Council BBS/E/B/0000L225Biotechnology and Biological Sciences Research Council BBSEB0000L967Biotechnology and Biological Sciences Research Council BBSEB0000L995Biotechnology and Biological Sciences Research Council BBS/E/B/000C0407Medical Research Council G0901338Medical Research Council G117/424Wellcome Trust 095691
6 · The paper itself

Abstract

PTEN, one of the most commonly mutated or lost tumor suppressors in human cancers, antagonizes signaling by the PI3K pathway. Mice with thymocyte-specific deletion of Pten rapidly develop peripheral lymphomas and autoimmunity, which may be caused by failed negative selection of thymocytes or from dysregulation of postthymic T cells. We induced conditional deletion of Pten from CD4 Th cells using a Cre knocked into the Tnfrsf4 (OX40) locus to generate OX40(Cre)Pten(f) mice. Pten-deficient Th cells proliferated more and produced greater concentrations of cytokines. The OX40(Cre)Pten(f) mice had a general increase in the number of lymphocytes in the lymph nodes, but not in the spleen. When transferred into wild-type (WT) mice, Pten-deficient Th cells enhanced anti-Listeria responses and the clearance of tumors under conditions in which WT T cells had no effect. Moreover, inflammatory responses were exaggerated and resolved later in OX40(Cre)Pten(f) mice than in WT mice. However, in contrast with models of thymocyte-specific Pten deletion, lymphomas and autoimmunity were not observed, even in older OX40(Cre)Pten(f) mice. Hence loss of Pten enhances Th cell function without obvious deleterious effects.

Indexed as

AnimalsAutoimmunityBlotting, WesternCD4-Positive T-LymphocytesFlow CytometryGene Knock-In TechniquesHomeostasisLymphocyte ActivationLymphomaMiceMice, TransgenicPTEN PhosphohydrolaseSignal TransductionPTEN PhosphohydrolasePten protein, mouse

Identifiers

PMID22611241
PMCPMC3378038
OpenAlexW2132579437

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.