Evidence map›Paper›PMID 29337666›Full record

ArticleeLife2018

Tuning of in vivo cognate B-T cell interactions by Intersectin 2 is required for effective anti-viral B cell immunity.

Marianne Burbage, Francesca Gasparrini, Shweta Aggarwal, Mauro Gaya, Johan Arnold, Usha Nair, Michael Way, Andreas Bruckbauer, Facundo D Batista

Open access · goldAbstract read
In one paragraph

Article in eLife, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
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  5. Article
  6. The Ins and Outs of Antigen Uptake in B cells.Frontiers in immunology · 2022
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
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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

9 authors at 2 institutions in 3 countries.

Marianne BurbageLymphocyte Biology Laboratory, The Francis Crick Institute, London, United Kingdom.ORCID 0000-0003-0686-2608
Francesca GasparriniLymphocyte Biology Laboratory, The Francis Crick Institute, London, United Kingdom.
Shweta AggarwalLymphocyte Biology Laboratory, The Francis Crick Institute, London, United Kingdom.
Mauro GayaLymphocyte Biology Laboratory, The Francis Crick Institute, London, United Kingdom.
Johan ArnoldRagon Institute of MGH, MIT and Harvard, Cambridge, United States.
Usha NairRagon Institute of MGH, MIT and Harvard, Cambridge, United States.
Michael WayCellular Signalling and Cytoskeletal Function Laboratory, The Francis Crick Institute, London, United Kingdom.
Andreas BruckbauerLymphocyte Biology Laboratory, The Francis Crick Institute, London, United Kingdom.
Facundo D BatistaLymphocyte Biology Laboratory, The Francis Crick Institute, London, United Kingdom.ORCID 0000-0002-1130-9463
The Francis Crick Institute · GBRagon Institute of MGH, MIT and Harvard · US

Funding

Support Component D/Vaccine Discovery, Concept to ClinicUM1AI100663 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI GODZIK, ADAM · 2012 to 2018
$131.5M
"Bottom - Up" Profiling of Interacting Cellular SystemsDP2GM119419 · NIGMS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI SHALEK, ALEX K · 2015 to 2015
$2.3M
An integrated multiplexed genomic assay for low input clinical samples1U24AI118672 · NIAID · BROAD INSTITUTE, INC. · PI SHALEK, ALEX K · 2015 to 2019
$2.0M
Cancer Research UK FC001035Cancer Research UK FC001209NIAID NIH HHS U24 AI118672NIAID NIH HHS UM1 AI100663NIGMS NIH HHS DP2 GM119419Wellcome Trust FC001035Wellcome Trust FC001209
6 · The paper itself

Abstract

Wiskott-Aldrich syndrome (WAS) is an immune pathology associated with mutations in WAS protein (WASp) or in WASp interacting protein (WIP). Together with the small GTPase Cdc42 and other effectors, these proteins participate in the remodelling of the actin network downstream of BCR engagement. Here we show that mice lacking the adaptor protein ITSN2, a G-nucleotide exchange factor (GEF) for Cdc42 that also interacts with WASp and WIP, exhibited increased mortality during primary infection, incomplete protection after Flu vaccination, reduced germinal centre formation and impaired antibody responses to vaccination. These defects were found, at least in part, to be intrinsic to the B cell compartment. In vivo, ITSN2 deficient B cells show a reduction in the expression of SLAM, CD84 or ICOSL that correlates with a diminished ability to form long term conjugates with T cells, to proliferate in vivo, and to differentiate into germinal centre cells. In conclusion, our study not only revealed a key role for ITSN2 as an important regulator of adaptive immune-response during vaccination and viral infection but it is also likely to contribute to a better understanding of human immune pathologies.

Indexed as

Adaptor Proteins, Vesicular TransportAnimalsB-LymphocytesCell AdhesionCell ProliferationInfluenza VaccinesMiceOrthomyxoviridaeOrthomyxoviridae InfectionsSurvival AnalysisT-LymphocytesAdaptor Proteins, Vesicular TransportInfluenza VaccinesItsn2 protein, mouseantibody responsesB cellsB-T interactionsimmunologymouseSLAM family receptorsWiskott-Aldrich syndrome

Identifiers

PMID29337666
PMCPMC5770159
OpenAlexW2783532479

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.