Evidence map›Paper›PMID 32324805›Full record

ArticlePLoS pathogens2020

The B-cell inhibitory receptor CD22 is a major factor in host resistance to Streptococcus pneumoniae infection.

Vitor E Fernandes, Giuseppe Ercoli, Alan Bénard, Carolin Brandl, Hannah Fahnenstiel, Jennifer Müller-Winkler, Georg F Weber, Paul Denny, Lars Nitschke, Peter W Andrew

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

6 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. An in vivo atlas of host-pathogen transcriptomes duringProceedings of the National Academy of Sciences of the United States of America · 2020
    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

10 authors at 4 institutions in 2 countries.

Vitor E FernandesDepartment of Infection, Immunity and Inflammation, University of Leicester, Leicester, United Kingdom.ORCID 0000-0001-5179-2122
Giuseppe ErcoliDepartment of Genetics, University of Leicester, Leicester, United Kingdom.ORCID 0000-0001-7326-1680
Alan BénardDepartment of Surgery, University Hospital Erlangen, Erlangen, Germany.ORCID 0000-0002-7175-813X
Carolin BrandlDivision of Genetics, Department of Biology, University of Erlangen, Erlangen, Germany.
Hannah FahnenstielDivision of Genetics, Department of Biology, University of Erlangen, Erlangen, Germany.
Jennifer Müller-WinklerDivision of Genetics, Department of Biology, University of Erlangen, Erlangen, Germany.
Georg F WeberDepartment of Surgery, University Hospital Erlangen, Erlangen, Germany.
Paul DennyMammalian Genetics Unit, Medical Research Council, Harwell, United Kingdom.
Lars NitschkeDivision of Genetics, Department of Biology, University of Erlangen, Erlangen, Germany.ORCID 0000-0001-7236-379X
Peter W AndrewDepartment of Infection, Immunity and Inflammation, University of Leicester, Leicester, United Kingdom.
Friedrich-Alexander-Universität Erlangen-Nürnberg · DEUniversity of Leicester · GBUniversitätsklinikum Erlangen · DEMedical Research Council · GB

Funding

Medical Research Council G0501416Medical Research Council MC_U142684174
6 · The paper itself

Abstract

Streptococcus pneumoniae is a major human pathogen, causing pneumonia and sepsis. Genetic components strongly influence host responses to pneumococcal infections, but the responsible loci are unknown. We have previously identified a locus on mouse chromosome 7 from a susceptible mouse strain, CBA/Ca, to be crucial for pneumococcal infection. Here we identify a responsible gene, Cd22, which carries a point mutation in the CBA/Ca strain, leading to loss of CD22 on B cells. CBA/Ca mice and gene-targeted CD22-deficient mice on a C57BL/6 background are both similarly susceptible to pneumococcal infection, as shown by bacterial replication in the lungs, high bacteremia and early death. After bacterial infections, CD22-deficient mice had strongly reduced B cell populations in the lung, including GM-CSF producing, IgM secreting innate response activator B cells, which are crucial for protection. This study provides striking evidence that CD22 is crucial for protection during invasive pneumococcal disease.

Indexed as

AnimalsBacteremiaB-LymphocytesFemaleHost-Pathogen InteractionsHumansMaleMiceMice, Inbred BALB CMice, Inbred C57BLMice, Inbred CBAPneumococcal InfectionsPneumonia, PneumococcalSialic Acid Binding Ig-like Lectin 2Streptococcus pneumoniaeSialic Acid Binding Ig-like Lectin 2

Identifiers

PMID32324805
PMCPMC7179836
OpenAlexW3020774706

What OpenQuestion holds

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LicenceCC BY
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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.