Evidence map›Paper›PMID 29146903›Full record

ArticleNature communications2017

Wiskott-Aldrich syndrome protein regulates autophagy and inflammasome activity in innate immune cells.

Pamela P Lee, Damián Lobato-Márquez, Nayani Pramanik, Andrea Sirianni, Vanessa Daza-Cajigal, Elizabeth Rivers, Alessia Cavazza, Gerben Bouma, Dale Moulding, Kjell Hultenby and 7 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

41 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Gene therapy for Whiskott-Aldrich syndrome: The latest news.Clinical and translational medicine · 2022
    Article
  18. Review
  19. Review
  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

17 authors at 7 institutions in 5 countries.

Pamela P LeeInfection, Immunity and Inflammation Program, Great Ormond Street Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH, UK.
Damián Lobato-MárquezSection of Microbiology, MRC Centre of Molecular Bacteriology and Infection, Imperial College London, Armstrong Road, London, SW7 2AZ, UK.
Nayani PramanikInfection, Immunity and Inflammation Program, Great Ormond Street Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH, UK.
Andrea SirianniSection of Microbiology, MRC Centre of Molecular Bacteriology and Infection, Imperial College London, Armstrong Road, London, SW7 2AZ, UK.
Vanessa Daza-CajigalUniversity College London Institute of Immunity and Transplantation, London, NW3 2PF, UK.
Elizabeth RiversInfection, Immunity and Inflammation Program, Great Ormond Street Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH, UK.
Alessia CavazzaInfection, Immunity and Inflammation Program, Great Ormond Street Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH, UK.
Gerben BoumaInfection, Immunity and Inflammation Program, Great Ormond Street Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH, UK.
Dale MouldingInfection, Immunity and Inflammation Program, Great Ormond Street Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH, UK.
Kjell HultenbyKarolinska Institutet, Department of Laboratory Medicine, 14186, Stockholm, Sweden.
Lisa S WesterbergKarolinska Institutet, Department of Microbiology, Tumor and Cell Biology, 171 77, Stockholm, Sweden.ORCID http://orcid.org/0000-0003-2943-2192
Michael HollinsheadDepartment of Pathology, University of Cambridge, Tennis Court Road, Cambridge, CB2 1AP, UK.
Yu-Lung LauDepartment of Paediatrics and Adolescent Medicine, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong, SAR, China.
Siobhan O BurnsInfection, Immunity and Inflammation Program, Great Ormond Street Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH, UK.
Serge MostowySection of Microbiology, MRC Centre of Molecular Bacteriology and Infection, Imperial College London, Armstrong Road, London, SW7 2AZ, UK.ORCID http://orcid.org/0000-0002-7286-6503
Mona Bajaj-ElliottInfection, Immunity and Inflammation Program, Great Ormond Street Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH, UK. m.bajaj-elliott@ucl.ac.uk.
Adrian J ThrasherInfection, Immunity and Inflammation Program, Great Ormond Street Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH, UK. a.thrasher@ucl.ac.uk.
University College London · GBImperial College London · GBChinese University of Hong Kong · HKKarolinska Institutet · SEGreat Ormond Street Hospital for Children NHS Foundation Trust · GBInstitute of Child Health · GRUniversity of Cambridge · GB

Funding

Wellcome TrustWellcome Trust 104807/Z/14/Z
6 · The paper itself

Abstract

Dysregulation of autophagy and inflammasome activity contributes to the development of auto-inflammatory diseases. Emerging evidence highlights the importance of the actin cytoskeleton in modulating inflammatory responses. Here we show that deficiency of Wiskott-Aldrich syndrome protein (WASp), which signals to the actin cytoskeleton, modulates autophagy and inflammasome function. In a model of sterile inflammation utilizing TLR4 ligation followed by ATP or nigericin treatment, inflammasome activation is enhanced in monocytes from WAS patients and in WAS-knockout mouse dendritic cells. In ex vivo models of enteropathogenic Escherichia coli and Shigella flexneri infection, WASp deficiency causes defective bacterial clearance, excessive inflammasome activation and host cell death that are associated with dysregulated septin cage-like formation, impaired autophagic p62/LC3 recruitment and defective formation of canonical autophagosomes. Taken together, we propose that dysregulation of autophagy and inflammasome activities contribute to the autoinflammatory manifestations of WAS, thereby identifying potential targets for therapeutic intervention.

Indexed as

Actin CytoskeletonAnimalsAutophagyBacterial LoadCell Line, TumorDendritic CellsEnteropathogenic Escherichia coliHumansImmunity, InnateInflammasomesInterferon Type IMiceMice, Inbred C57BLMice, KnockoutMonocytesNigericinInflammasomesInterferon Type INigericinNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanSeptinsTLR4 protein, humanToll-Like Receptor 4WAS protein, humanWas protein, mouseWiskott-Aldrich Syndrome Protein

Identifiers

PMID29146903
PMCPMC5691069
OpenAlexW2768429539

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.