Evidence map›Paper›PMID 26740009›Full record

ArticleImmunology and cell biology2016

PI3Kδ promotes CD4(+) T-cell interactions with antigen-presenting cells by increasing LFA-1 binding to ICAM-1.

Fabien Garçon, Klaus Okkenhaug

Open access · hybridAbstract read
In one paragraph

Article in Immunology and cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

20 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. PI3K in T Cell Adhesion and Trafficking.Frontiers in immunology · 2021
    Review
  13. β2 Integrins-Multi-Functional Leukocyte Receptors in Health and Disease.International journal of molecular sciences · 2020
    Review
  14. Integrin crosstalk allows CD4+ T lymphocytes to continue migrating in the upstream direction after flow.Integrative biology : quantitative biosciences from nano to macro · 2019
    Article
  15. Review
  16. Review
  17. Article
  18. LFA-1 in T Cell Migration and Differentiation.Frontiers in immunology · 2018
    Review
  19. Combined BTK and PI3Kδ Inhibition with Acalabrutinib and ACP-319 Improves Survival and Tumor Control in CLL Mouse Model.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017
    Article
  20. 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

2 authors at 1 institution in 1 country.

Fabien GarçonLaboratory of Lymphocyte Signaling and Development, The Babraham Institute, Babraham Research Campus, Cambridge, UK.
Klaus OkkenhaugLaboratory of Lymphocyte Signaling and Development, The Babraham Institute, Babraham Research Campus, Cambridge, UK.ORCID 0000-0002-9432-4051
Babraham Institute · GB

Funding

Biotechnology and Biological Sciences Research Council BB/F015461/1Biotechnology and Biological Sciences Research Council BBS/E/B/000C0407Biotechnology and Biological Sciences Research Council BBS/E/B/000C0409Wellcome Trust 095691
6 · The paper itself

Abstract

Activation of T lymphocytes by peptide/major histocompatibility complex on antigen-presenting cells (APCs) involves dynamic contacts between the two cells, during which T cells undergo marked morphological changes. These interactions are facilitated by integrins. Activation of the T cells increases the binding of the integrin lymphocyte function-associated antigen 1 (LFA-1) expressed by T cells to intercellular adhesion molecule (ICAM)-1 and ICAM-2 expressed by APCs. The signalling pathways that control integrin affinities are incompletely defined. The phosphoinositide 3-kinases (PI3Ks) generate second-messenger signalling molecules that control cell growth, proliferation, differentiation and trafficking. Here we show that in T cells, PI3Kδ attenuates the activation of Rac1, but sustains the activation of Rap1. Consequently, PI3Kδ increases LFA-1-dependent adhesion to form stable conjugates with APCs. Increased Rap1 activity and LFA-1 adhesion were only in part mediated by the downstream kinase Akt, suggesting the involvement of additional phosphatidylinositol(3,4,5)P3-binding proteins. These results establish a link between PI3K activity, cytoskeletal changes and integrin binding and help explain the impaired T-cell-dependent immune responses in PI3Kδ-deficient mice.

Indexed as

Cell CommunicationActin Depolymerizing FactorsAnimalsAntigen-Presenting CellsCD4-Positive T-LymphocytesCell AdhesionCell MovementCell ShapeClass I Phosphatidylinositol 3-KinasesDendritic CellsGTP-Binding ProteinsIntercellular Adhesion Molecule-1Lymph NodesLymphocyte Function-Associated Antigen-1Mice, Inbred C57BLPhosphatidylinositol 3-KinasesActin Depolymerizing FactorsClass I Phosphatidylinositol 3-KinasesGTP-Binding ProteinsIntercellular Adhesion Molecule-1Lymphocyte Function-Associated Antigen-1Phosphatidylinositol 3-KinasesPik3cd protein, mouseProto-Oncogene Proteins c-aktReceptors, Antigen, T-Cell

Identifiers

PMID26740009
PMCPMC4829101
OpenAlexW2287984141

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.