Evidence map›Paper›PMID 26965188›Full record

ArticleNature communications2016

αv Integrins combine with LC3 and atg5 to regulate Toll-like receptor signalling in B cells.

Mridu Acharya, Anna Sokolovska, Jenny M Tam, Kara L Conway, Caroline Stefani, Fiona Raso, Subhankar Mukhopadhyay, Marianela Feliu, Elahna Paul, John Savill and 5 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing 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

40 citing papers in PubMed, 62 citations in OpenAlex.

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

15 authors at 5 institutions in 2 countries.

Mridu AcharyaImmunology Program, Benaroya Research Institute, 1201 Ninth Avenue, Seattle, Washington 98101, USA.
Anna SokolovskaLaboratory of Developmental Immunology, Department of Pediatrics, Massachusetts General Hospital/ Harvard Medical School, 55 Fruit Street, Boston, Massachusetts 02114, USA.
Jenny M TamDivision of Infectious Disease, Department of Medicine, , Massachusetts General Hospital/ Harvard Medical School, 55 Fruit Street, Boston, Massachusetts 02114, USA.
Kara L ConwayGastrointestinal Unit and Center for the Study of Inflammatory Bowel Disease, Massachusetts General Hospital/ Harvard Medical School, 55 Fruit Street, Boston, Massachusetts 02114, USA.
Caroline StefaniImmunology Program, Benaroya Research Institute, 1201 Ninth Avenue, Seattle, Washington 98101, USA.
Fiona RasoImmunology Program, Benaroya Research Institute, 1201 Ninth Avenue, Seattle, Washington 98101, USA.
Subhankar MukhopadhyayMicrobial Pathogenesis Group, Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK.
Marianela FeliuLaboratory of Developmental Immunology, Department of Pediatrics, Massachusetts General Hospital/ Harvard Medical School, 55 Fruit Street, Boston, Massachusetts 02114, USA.
Elahna PaulLaboratory of Developmental Immunology, Department of Pediatrics, Massachusetts General Hospital/ Harvard Medical School, 55 Fruit Street, Boston, Massachusetts 02114, USA.
John SavillMRC/University of Edinburgh Centre for Inflammation Research, 47 Little France Crescent, Edinburgh EH16 4TJ, UK.
Richard O HynesHoward Hughes Medical Institute, Koch Institute of Integrated Cancer Biology, Massachusetts Institute for Technology, Cambridge, 500 Main Street, Cambridge, Massachusetts 02139, USA.
Ramnik J XavierDivision of Infectious Disease, Department of Medicine, , Massachusetts General Hospital/ Harvard Medical School, 55 Fruit Street, Boston, Massachusetts 02114, USA.
Jatin M VyasDivision of Infectious Disease, Department of Medicine, , Massachusetts General Hospital/ Harvard Medical School, 55 Fruit Street, Boston, Massachusetts 02114, USA.ORCID http://orcid.org/0000-0002-9985-9565
Lynda M StuartImmunology Program, Benaroya Research Institute, 1201 Ninth Avenue, Seattle, Washington 98101, USA.
Adam Lacy-HulbertImmunology Program, Benaroya Research Institute, 1201 Ninth Avenue, Seattle, Washington 98101, USA.
Harvard University · USCenter for Infectious Disease Research · USCentre for Inflammation Research · GBHoward Hughes Medical Institute · USWellcome Sanger Institute · GB

Funding

Pilot & Feasibility ProgramP30DK043351 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI RAYMOND T CHUNG · 1991 to 2026
$35.3M
Genetic and Pathway Analysis CoreU19AI109725 · NIAID · WASHINGTON UNIVERSITY · PI XAVIER, RAMNIK J · 2014 to 2018
$32.7M
The role of the phagosome in innate immune sensingR01AI079198 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI STUART, LYNDA · 2008 to 2012
$2.4M
Functional Role of the Tetraspanin CD82/Kai1 in Innate and Adaptive ImmunityR01AI092084 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI VYAS, JATIN M · 2011 to 2015
$2.2M
The role of TLR9 on Aspergillus fumigatus phagosomesR01AI097519 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI VYAS, JATIN M · 2013 to 2016
$1.6M
Dendritic Cell Control of Intestinal T Cell ResponsesR01DK093695 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI LACY-HULBERT, ADAM · 2012 to 2015
$1.4M
Howard Hughes Medical InstituteMedical Research Council G0802069NIAID NIH HHS AI079198NIAID NIH HHS R01 AI079198NIDDK NIH HHS DK093695NIDDK NIH HHS R01 DK093695Wellcome Trust 34561
6 · The paper itself

Abstract

Integrin signalling triggers cytoskeletal rearrangements, including endocytosis and exocytosis of integrins and other membrane proteins. In addition to recycling integrins, this trafficking can also regulate intracellular signalling pathways. Here we describe a role for αv integrins in regulating Toll-like receptor (TLR) signalling by modulating intracellular trafficking. We show that deletion of αv or β3 causes increased B-cell responses to TLR stimulation in vitro, and αv-conditional knockout mice have elevated antibody responses to TLR-ligand-associated antigens. αv regulates TLR signalling by promoting recruitment of the autophagy component LC3 (microtubule-associated proteins 1 light chain 3) to TLR-containing endosomes, which is essential for progression from NF-κB to IRF signalling, and ultimately for traffic to lysosomes where signalling is terminated. Disruption of LC3 recruitment leads to prolonged NF-κB signalling and increased B-cell proliferation and antibody production. This work identifies a previously unrecognized role for αv and the autophagy components LC3 and atg5 in regulating TLR signalling and B-cell immunity.

Indexed as

AnimalsAutophagyAutophagy-Related Protein 5Blotting, WesternB-LymphocytesCell ProliferationEnzyme-Linked Immunosorbent AssayFlow CytometryIntegrin alphaVIntegrin beta3In Vitro TechniquesMiceMice, KnockoutMicroscopy, ConfocalMicrotubule-Associated ProteinsProtein TransportAtg5 protein, mouseAutophagy-Related Protein 5Integrin alphaVIntegrin beta3Map1lc3b protein, mouseMicrotubule-Associated ProteinsToll-Like Receptors

Identifiers

PMID26965188
PMCPMC4792966
OpenAlexW2295020433

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.