Evidence map›Paper›PMID 34445732›Full record

ArticleInternational journal of molecular sciences2021

Involvement of Virus-Induced Interferon Production in IgG Autoantibody-Mediated Anemia.

Sarah Legrain, Dan Su, Mélanie Gaignage, Cor Breukel, Jill Claassens, Conny Brouwers, Margot M Linssen, Shozo Izui, J Sjef Verbeek, Jean-Paul Coutelier

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 51% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. International journal of molecular sciences · 2023
    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 3 countries.

Sarah LegrainUnit of Experimental Medicine, de Duve Institute, Université Catholique de Louvain, 1200 Bruxelles, Belgium.
Dan SuUnit of Experimental Medicine, de Duve Institute, Université Catholique de Louvain, 1200 Bruxelles, Belgium.
Mélanie GaignageUnit of Experimental Medicine, de Duve Institute, Université Catholique de Louvain, 1200 Bruxelles, Belgium.
Cor BreukelDepartment of Human Genetics, Leiden University Medical Center, 2300 RC Leiden, The Netherlands.
Jill ClaassensDepartment of Human Genetics, Leiden University Medical Center, 2300 RC Leiden, The Netherlands.
Conny BrouwersDepartment of Human Genetics, Leiden University Medical Center, 2300 RC Leiden, The Netherlands.
Margot M LinssenDepartment of Human Genetics, Leiden University Medical Center, 2300 RC Leiden, The Netherlands.
Shozo IzuiDepartment of Pathology and Immunology, Centre Médical Universitaire, University of Geneva, 4 1211 Geneva, Switzerland.
J Sjef VerbeekDepartment of Human Genetics, Leiden University Medical Center, 2300 RC Leiden, The Netherlands.
Jean-Paul CoutelierUnit of Experimental Medicine, de Duve Institute, Université Catholique de Louvain, 1200 Bruxelles, Belgium.
Leiden University Medical Center · NLde Duve Institute · BEUCLouvain · BEUniversity of Geneva · CH

Funding

Fonds De La Recherche Scientifique - FNRS salaryFrench Community (Belgium) action de recherche concertée
6 · The paper itself

Abstract

Infection with viruses, such as the lactate dehydrogenase-elevating virus (LDV), is known to trigger the onset of autoimmune anemia through the enhancement of the phagocytosis of autoantibody-opsonized erythrocytes by activated macrophages. Type I interferon receptor-deficient mice show enhanced anemia, which suggests a protective effect of these cytokines, partly through the control of type II interferon production. The development of anemia requires the expression of Fcγ receptors (FcγR) I, III, and IV. Whereas LDV infection decreases FcγR III expression, it enhances FcγR I and IV expression in wild-type animals. The LDV-associated increase in the expression of FcγR I and IV is largely reduced in type I interferon receptor-deficient mice, through both type II interferon-dependent and -independent mechanisms. Thus, the regulation of the expression of FcγR I and IV, but not III, by interferons may partly explain the exacerbating effect of LDV infection on anemia that results from the enhanced phagocytosis of IgG autoantibody-opsonized erythrocytes.

Indexed as

Anemia, Hemolytic, AutoimmuneAnimalsArterivirus InfectionsHost-Pathogen InteractionsInterferonsLactate dehydrogenase-elevating virusMiceMice, Inbred C57BLMice, KnockoutPhagocytosisReceptors, IgGInterferonsReceptors, IgGautoimmune anemiaFc receptorsinterferonlactate dehydrogenase-elevating virus

Identifiers

PMID34445732
PMCPMC8396558
OpenAlexW3193761019

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.