Evidence map›Paper›PMID 27425374›Full record

ArticleNature communications2016

Deletion of Wiskott-Aldrich syndrome protein triggers Rac2 activity and increased cross-presentation by dendritic cells.

Marisa A P Baptista, Marton Keszei, Mariana Oliveira, Karen K S Sunahara, John Andersson, Carin I M Dahlberg, Austen J Worth, Agne Liedén, I-Chun Kuo, Robert P A Wallin and 10 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 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.1field-weighted citation impact, top 9% 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, 36 citations in OpenAlex.

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  20. Dendritic cell analysis in primary immunodeficiency.Current opinion in allergy and clinical immunology · 2016
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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

20 authors at 7 institutions in 6 countries.

Marisa A P BaptistaDepartment of Microbiology Tumor and Cell biology, Karolinska Institutet, Stockholm 171 77, Sweden.
Marton KeszeiDepartment of Microbiology Tumor and Cell biology, Karolinska Institutet, Stockholm 171 77, Sweden.
Mariana OliveiraDepartment of Microbiology Tumor and Cell biology, Karolinska Institutet, Stockholm 171 77, Sweden.
Karen K S SunaharaDepartment of Microbiology Tumor and Cell biology, Karolinska Institutet, Stockholm 171 77, Sweden.
John AnderssonDepartment of Medicine Solna, Translational Immunology Unit, Karolinska Institutet and Karolinska University Hospital, Stockholm 171 76, Sweden.
Carin I M DahlbergDepartment of Microbiology Tumor and Cell biology, Karolinska Institutet, Stockholm 171 77, Sweden.
Austen J WorthUniversity College London Institute of Child Health, London WC1N 1EH, UK.
Agne LiedénDepartment of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm 171 76, Sweden.
I-Chun KuoDepartment of Paediatrics, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 119228, Singapore.
Robert P A WallinDepartment of Microbiology Tumor and Cell biology, Karolinska Institutet, Stockholm 171 77, Sweden.
Scott B SnapperGastroenterology Division, Children's Hospital, Harvard Medical School, Boston MA 02115, USA.
Liv EidsmoDepartment of Medicine Solna, Dermatology and Venereology Unit, Karolinska Institutet, Stockholm 171 76, Sweden.
Annika ScheyniusDepartment of Medicine Solna, Translational Immunology Unit, Karolinska Institutet and Karolinska University Hospital, Stockholm 171 76, Sweden.
Mikael C I KarlssonDepartment of Microbiology Tumor and Cell biology, Karolinska Institutet, Stockholm 171 77, Sweden.ORCID 0000-0001-5582-614X
Gerben BoumaUniversity College London Institute of Child Health, London WC1N 1EH, UK.
Siobhan O BurnsUniversity College London Institute of Child Health, London WC1N 1EH, UK.
Mattias N E ForsellDepartment of Microbiology Tumor and Cell biology, Karolinska Institutet, Stockholm 171 77, Sweden.
Adrian J ThrasherUniversity College London Institute of Child Health, London WC1N 1EH, UK.
Susanne NylénDepartment of Microbiology Tumor and Cell biology, Karolinska Institutet, Stockholm 171 77, Sweden.
Lisa S WesterbergDepartment of Microbiology Tumor and Cell biology, Karolinska Institutet, Stockholm 171 77, Sweden.ORCID 0000-0003-2943-2192
Karolinska Institutet · SEUniversity College London · GBKarolinska University Hospital · SEBoston Children's Hospital · USNational University of Singapore · SGRoyal Free London NHS Foundation Trust · GBUniversity of Würzburg · DE

Funding

STRUCTURE-FUNCTION RELATIONSHIPS IN THE ALIMENTARY TRACTP30DK034854 · NIDDK · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI WAYNE I LENCER · 1986 to 2026
$32.4M
WIP in TCR signaling and actin reorganizationP01HL059561 · NHLBI · IMMUNE DISEASE INSTITUTE, INC. · PI GEHA, RAIF SALIM · 1997 to 2012
$21.8M
The Pathogenesis Of Colitis In A Novel Th2 Model Of IBDR01AI050950 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI SNAPPER, SCOTT B · 2002 to 2013
$2.6M
NHLBI NIH HHS P01 HL059561NIAID NIH HHS R01 AI050950NIDDK NIH HHS P30 DK034854Wellcome Trust
6 · The paper itself

Abstract

Wiskott-Aldrich syndrome (WAS) is caused by loss-of-function mutations in the WASp gene. Decreased cellular responses in WASp-deficient cells have been interpreted to mean that WASp directly regulates these responses in WASp-sufficient cells. Here, we identify an exception to this concept and show that WASp-deficient dendritic cells have increased activation of Rac2 that support cross-presentation to CD8(+) T cells. Using two different skin pathology models, WASp-deficient mice show an accumulation of dendritic cells in the skin and increased expansion of IFNγ-producing CD8(+) T cells in the draining lymph node and spleen. Specific deletion of WASp in dendritic cells leads to marked expansion of CD8(+) T cells at the expense of CD4(+) T cells. WASp-deficient dendritic cells induce increased cross-presentation to CD8(+) T cells by activating Rac2 that maintains a near neutral pH of phagosomes. Our data reveals an intricate balance between activation of WASp and Rac2 signalling pathways in dendritic cells.

Indexed as

Gene DeletionAnimalsAntigens, DermatophagoidesArthropod ProteinsCD8-Positive T-LymphocytesCell ProliferationCross-PrimingDendritic CellsInterferon-gammaLeishmania majorLymphocyte CountMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutPhagosomesProtein DomainsAntigens, DermatophagoidesArthropod ProteinsDermatophagoides pteronyssinus antigen p 2Interferon-gammaRAC2 GTP-Binding Proteinrac GTP-Binding ProteinsReactive Oxygen SpeciesWiskott-Aldrich Syndrome Protein

Identifiers

PMID27425374
PMCPMC4960314
OpenAlexW2489225126

What OpenQuestion holds

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Registered trials

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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.