Evidence map›Paper›PMID 25644899›Full record

ArticleNature communications2015

Toll-like receptor ligands sensitize B-cell receptor signalling by reducing actin-dependent spatial confinement of the receptor.

Spencer A Freeman, Valentin Jaumouillé, Kate Choi, Brian E Hsu, Harikesh S Wong, Libin Abraham, Marcia L Graves, Daniel Coombs, Calvin D Roskelley, Raibatak Das and 2 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

46 citing papers in PubMed, 84 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 3 institutions in 2 countries.

Spencer A Freeman1] Department of Microbiology &Immunology, University of British Columbia, 2350 Health Sciences Mall, Vancouver, British Columbia, Canada V6T 1Z3 [2] Department of Cellular &Physiological Sciences, University of British Columbia, 2350 Health Sciences Mall, Vancouver, British Columbia, Canada V6T 1Z3 [3] Life Sciences Institute I3 and Cell Research Groups, University of British Columbia, 2350 Health Sciences Mall, Vancouver, British Columbia, Canada V6T 1Z3 [4] Program in Cell Biology, The Hospital for Sick Kids Research Institute, 686 Bay Street, Toronto, Ontario, Canada M5G 0A4.
Valentin JaumouilléProgram in Cell Biology, The Hospital for Sick Kids Research Institute, 686 Bay Street, Toronto, Ontario, Canada M5G 0A4.
Kate Choi1] Department of Microbiology &Immunology, University of British Columbia, 2350 Health Sciences Mall, Vancouver, British Columbia, Canada V6T 1Z3 [2] Life Sciences Institute I3 and Cell Research Groups, University of British Columbia, 2350 Health Sciences Mall, Vancouver, British Columbia, Canada V6T 1Z3.
Brian E Hsu1] Department of Microbiology &Immunology, University of British Columbia, 2350 Health Sciences Mall, Vancouver, British Columbia, Canada V6T 1Z3 [2] Life Sciences Institute I3 and Cell Research Groups, University of British Columbia, 2350 Health Sciences Mall, Vancouver, British Columbia, Canada V6T 1Z3.
Harikesh S WongProgram in Cell Biology, The Hospital for Sick Kids Research Institute, 686 Bay Street, Toronto, Ontario, Canada M5G 0A4.
Libin Abraham1] Department of Microbiology &Immunology, University of British Columbia, 2350 Health Sciences Mall, Vancouver, British Columbia, Canada V6T 1Z3 [2] Life Sciences Institute I3 and Cell Research Groups, University of British Columbia, 2350 Health Sciences Mall, Vancouver, British Columbia, Canada V6T 1Z3 [3] Department of Mathematics and Institute of Applied Mathematics, 1984 Mathematics Road, University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z2.
Marcia L Graves1] Department of Microbiology &Immunology, University of British Columbia, 2350 Health Sciences Mall, Vancouver, British Columbia, Canada V6T 1Z3 [2] Department of Cellular &Physiological Sciences, University of British Columbia, 2350 Health Sciences Mall, Vancouver, British Columbia, Canada V6T 1Z3 [3] Life Sciences Institute I3 and Cell Research Groups, University of British Columbia, 2350 Health Sciences Mall, Vancouver, British Columbia, Canada V6T 1Z3.
Daniel CoombsDepartment of Mathematics and Institute of Applied Mathematics, 1984 Mathematics Road, University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z2.
Calvin D Roskelley1] Department of Cellular &Physiological Sciences, University of British Columbia, 2350 Health Sciences Mall, Vancouver, British Columbia, Canada V6T 1Z3 [2] Life Sciences Institute I3 and Cell Research Groups, University of British Columbia, 2350 Health Sciences Mall, Vancouver, British Columbia, Canada V6T 1Z3.
Raibatak DasDepartment of Integrative Biology, University of Colorado Denver, 1151 Arapahoe, Denver, Colorado 80204, USA.
Sergio GrinsteinProgram in Cell Biology, The Hospital for Sick Kids Research Institute, 686 Bay Street, Toronto, Ontario, Canada M5G 0A4.
Michael R Gold1] Department of Microbiology &Immunology, University of British Columbia, 2350 Health Sciences Mall, Vancouver, British Columbia, Canada V6T 1Z3 [2] Life Sciences Institute I3 and Cell Research Groups, University of British Columbia, 2350 Health Sciences Mall, Vancouver, British Columbia, Canada V6T 1Z3.
University of British Columbia · CAHospital for Sick Children · CAUniversity of Colorado Denver · US

Funding

Canadian Institutes of Health Research MOP-102474Canadian Institutes of Health Research MOP-68865
6 · The paper itself

Abstract

Integrating signals from multiple receptors allows cells to interpret the physiological context in which a signal is received. Here we describe a mechanism for receptor crosstalk in which receptor-induced increases in actin dynamics lower the threshold for signalling by another receptor. We show that the Toll-like receptor ligands lipopolysaccharide and CpG DNA, which are conserved microbial molecules, enhance signalling by the B-cell antigen receptor (BCR) by activating the actin-severing protein cofilin. Single-particle tracking reveals that increased severing of actin filaments reduces the spatial confinement of the BCR within the plasma membrane and increases BCR mobility. This allows more frequent collisions between BCRs and greater signalling in response to low densities of membrane-bound antigen. These findings implicate actin dynamics as a means of tuning receptor signalling and as a mechanism by which B cells distinguish inert antigens from those that are accompanied by indicators of microbial infection.

Indexed as

ActinsAnimalsImmunoblottingLigandsLipopolysaccharidesMiceMice, Inbred C57BLMicroscopy, ConfocalReceptors, Antigen, B-CellSignal TransductionToll-Like ReceptorsActinsLigandsLipopolysaccharidesReceptors, Antigen, B-CellToll-Like Receptors

Identifiers

PMID25644899
PMCPMC4327415
OpenAlexW2045054556

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.