Evidence map›Paper›PMID 25468342›Full record

ArticleBiophysical journal2014

Ligand-mediated friction determines morphodynamics of spreading T cells.

Pierre Dillard, Rajat Varma, Kheya Sengupta, Laurent Limozin

Abstract read
In one paragraph

Article in Biophysical journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
–field-weighted citation impact
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

24 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Antigen mobility regulates the dynamics and precision of antigen capture in the B cell immune synapse.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Mechanosurveillance: Tiptoeing T Cells.Frontiers in immunology · 2022
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Biphasic mechanosensitivity of T cell receptor-mediated spreading of lymphocytes.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  19. Article
  20. 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

4 authors.

Pierre DillardAdhesion & Inflammation, Aix-Marseille University, Inserm UMR 1067, CNRS UMR 7333, Marseille, France; CINAM, Aix-Marseille University, CNRS UMR 7325, Marseille, France.
Rajat VarmaLaboratory of Systems Biology, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD.
Kheya SenguptaCINAM, Aix-Marseille University, CNRS UMR 7325, Marseille, France. Electronic address: sengupta@cinam.univ-mrs.fr.
Laurent LimozinAdhesion & Inflammation, Aix-Marseille University, Inserm UMR 1067, CNRS UMR 7333, Marseille, France. Electronic address: laurent.limozin@inserm.fr.

Funding

European Research Council 307104Intramural NIH HHS
6 · The paper itself

Abstract

Spreading of T cells on antigen presenting cells is a crucial initial step in immune response. Spreading occurs through rapid morphological changes concomitant with the reorganization of surface receptors and of the cytoskeleton. Ligand mobility and frictional coupling of receptors to the cytoskeleton were separately recognized as important factors but a systematic study to explore their biophysical role in spreading was hitherto missing. To explore the impact of ligand mobility, we prepared chemically identical substrates on which molecules of anti-CD3 (capable of binding and activating the T cell receptor complex), were either immobilized or able to diffuse. We quantified the T cell spreading area and cell edge dynamics using quantitative reflection interference contrast microscopy, and imaged the actin distribution. On mobile ligands, as compared to fixed ligands, the cells spread much less, the actin is centrally, rather than peripherally distributed and the edge dynamics is largely altered. Blocking myosin-II or adding molecules of ICAM1 on the substrate largely abrogates these differences. We explain these observations by building a model based on the balance of forces between activation-dependent actin polymerization and actomyosin-generated tension on one hand, and on the frictional coupling of the ligand-receptor complexes with the actin cytoskeleton, the membrane and the substrate, on the other hand. Introducing the measured edge velocities in the model, we estimate the coefficient of frictional coupling between T Cell receptors or LFA-1 and the actin cytoskeleton. Our results provide for the first time, to our knowledge, a quantitative framework bridging T cell-specific biology with concepts developed for integrin-based mechanisms of spreading.

Indexed as

Cell MovementCell ShapeFrictionActin-Related Protein 2-3 ComplexActinsHumansIntercellular Adhesion Molecule-1Jurkat CellsLigandsMyosin Type IIPseudopodiaT-LymphocytesActin-Related Protein 2-3 ComplexActinsIntercellular Adhesion Molecule-1LigandsMyosin Type II

Identifiers

PMID25468342
PMCPMC4255222

What OpenQuestion holds

Textmetadata
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.