Evidence map›Paper›PMID 33226189›Full record

ArticleImmunity, inflammation and disease2021

Enhanced IgG

Jennifer Jaufmann, Melanie Carevic, Leyla Tümen, Derya Eliacik, Fee Schmitt, Dominik Hartl, Sandra Beer-Hammer

Open access · goldAbstract read
In one paragraph

Article in Immunity, inflammation and disease, 2021. 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
0.5field-weighted citation impact, top 32% 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.

  1. Article
  2. Article
  3. Enhanced IgGImmunity, inflammation and disease · 2021
    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

7 authors at 3 institutions in 2 countries.

Jennifer JaufmannDepartment of Pharmacology, Experimental Therapy, and Toxicology, Institute of Experimental and Clinical Pharmacology and Pharmacogenomik and ICePhA, University of Tuebingen, Tuebingen, Germany.
Melanie CarevicChildren's Hospital and Interdisciplinary Center for Infectious Diseases, 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.
Derya EliacikDepartment 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.
Dominik HartlChildren's Hospital and Interdisciplinary Center for Infectious Diseases, University of Tuebingen, Tuebingen, 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 · DENovartis (Switzerland) · CHUniversity Children's Hospital Tübingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChemokine receptors and their corresponding ligands are key players of immunity by regulation of immune cell differentiation and migration. CXCR1 is a high-affinity receptor for CXCL8. Differential expression of CXCR1 is associated with a variety of human pathologies including cancer and inflammatory diseases. While various studies have highlighted the importance of CXCR1-mediated CXCL8-sensing for neutrophil trafficking and function, its role in B-cell responses remains unsolved. Therefore, our aim was to investigate innate and adaptive antibody responses in CXCR1-deficient mice.

methodsCell populations of the spleen and the peritoneal cavity were identified and quantified via flow cytometry. To investigate thymus-independent (TI) and thymus-dependent (TD) antibody responses, mice were immunized intraperitoneally with TNP-Ficoll, Pneumovax23, and TNP-Chicken Gamma Globulin. Mice were bled before as well as 7 and 14 days after vaccination to collect serum. Serum antibody levels overtime were analyzed according to their specificity by enzyme-linked immunosorbent assay. B-1 cell functionality was examined by IL-5/IL-5Rα-dependent stimulation of peritoneal and splenic cells in vitro. To analyze CXCR1/2-expression, CD19

resultsThe distribution of natural B-1 cell populations was disturbed in the absence of CXCR1, while their responsiveness towards TI antigens and in vitro stimulation remained functional. Besides, CXCR1-deficiency was accompanied by increased frequencies of follicular B-2 cells in the spleen. Interestingly, these mice produced elevated levels of antigen-specific IgG

conclusionOur data demonstrate a previously unknown relevance of CXCR1 for the production of specific IgG

Indexed as

Antibody FormationAntigens, T-IndependentAnimalsImmunizationImmunoglobulin GMiceVaccinationAntigens, T-IndependentImmunoglobulin GB-1 cellsB-2 cellschemokine receptorsCXCR1germinal center reactioninnate and adaptive antibody responsesvaccination

Identifiers

PMID33226189
PMCPMC7860589
OpenAlexW3109782950

What OpenQuestion holds

Textmetadata
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.