Evidence map›Paper›PMID 33098380›Full record

ArticleImmunity, inflammation and disease2020

SLy2-deficiency promotes B-1 cell immunity and triggers enhanced production of IgM and IgG

Jennifer Jaufmann, Leyla Tümen, Fee Schmitt, Daniel Schäll, Max von Holleben, Sandra Beer-Hammer

Open access · goldAbstract read
In one paragraph

Article in Immunity, inflammation and disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.3field-weighted citation impact, top 38% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Jennifer JaufmannDepartment of Pharmacology, Experimental Therapy and Toxicology, Institute of Experimental and Clinical Pharmacology and Pharmacogenomik and ICePhA, University of Tuebingen, Tuebingen, Germany.
Leyla TümenDepartment of Pharmacology, Experimental Therapy and Toxicology, Institute of Experimental and Clinical Pharmacology and Pharmacogenomik and ICePhA, University of Tuebingen, Tuebingen, Germany.
Fee SchmittDepartment of Pharmacology, Experimental Therapy and Toxicology, Institute of Experimental and Clinical Pharmacology and Pharmacogenomik and ICePhA, University of Tuebingen, Tuebingen, Germany.
Daniel SchällDepartment of Pharmacology, Experimental Therapy and Toxicology, Institute of Experimental and Clinical Pharmacology and Pharmacogenomik and ICePhA, University of Tuebingen, Tuebingen, Germany.
Max von HollebenInstitute for Medical Microbiology and Hospital Hygiene, Heinrich-Heine-University, Duesseldorf, Germany.
Sandra Beer-HammerDepartment of Pharmacology, Experimental Therapy and Toxicology, Institute of Experimental and Clinical Pharmacology and Pharmacogenomik and ICePhA, University of Tuebingen, Tuebingen, Germany.ORCID 0000-0001-6049-0257
University of Tübingen · DEHeinrich Heine University Düsseldorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDespite the benefits of existing vaccines, Streptococcus pneumoniae is still responsible for the greatest proportion of respiratory tract infections around the globe, thereby substantially contributing to morbidity and mortality in humans. B-1 cells are key players of bacterial clearance during pneumococcal infection and even provide long-lasting immunity towards S. pneumoniae. Previous reports strongly suggest an essential role of the immunoinhibitory adapter Src homology domain 3 lymphocyte protein 2 (SLy2) for B-1 cell-mediated antibody production. The objective of this study is to evaluate S. pneumoniae-directed B cell responses in the context of SLy2 deficiency.

methodsB-1 cell populations were analyzed via flow cytometry before and after pneumococcal immunization of SLy2-deficient and wild-type control mice. Global and vaccine-specific immunoglobulin M (IgM) and IgG antibody titers were assessed by enzyme-linked immunosorbent assay. To investigate survival rates during acute pneumococcal lung infection, mice were intranasally challenged with S. pneumoniae (serotype 3). Complementary isolated splenic B cells were stimulated in vitro and their proliferative response was assessed by fluorescent staining. In vitro antibody secretion was quantified by LEGENDplex.

resultsWe demonstrate increased frequencies of B-1 cells and elevated titers of preantigenic IgM in SLy2-deficient mice. In addition, these mice produce significantly more amounts of IgM and IgG

conclusionOur results reveal reinforced specific antibody responses towards pneumococcal polysaccharides and enhanced IgG

Indexed as

B-Lymphocyte SubsetsPneumococcal VaccinesAdaptor Proteins, Vesicular TransportAnimalsAntibodies, BacterialEscherichia coliFemaleImmunoglobulin GImmunoglobulin MMaleMiceMice, Inbred C57BLAdaptor Proteins, Vesicular TransportAntibodies, BacterialImmunoglobulin GImmunoglobulin MPneumococcal VaccinesSLy2 protein, mouseantibody responsesB-1 cellsnatural IgMpneumococcal vaccinationpneumoniaSrc homology domain 3 lymphocyte protein 2Streptococcus pneumoniae

Identifiers

PMID33098380
PMCPMC7654406
OpenAlexW3093941598

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.