Evidence map›Paper›PMID 33912177›Full record

ArticleFrontiers in immunology2021

Lack of Cell Cycle Inhibitor p21 and Low CD4

Jop Jans, Wendy W Unger, Elisabeth A M Raeven, Elles R Simonetti, Marc J Eleveld, Ronald de Groot, Marien I de Jonge, Gerben Ferwerda

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

Article in Frontiers in immunology, 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 61% 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. 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

8 authors at 3 institutions in 1 country.

Jop JansLaboratory of Pediatrics, Division of Pediatric Infectious Diseases and Immunology, Erasmus MC University Medical Center-Sophia Children's Hospital, Rotterdam, Netherlands.
Wendy W UngerLaboratory of Pediatrics, Division of Pediatric Infectious Diseases and Immunology, Erasmus MC University Medical Center-Sophia Children's Hospital, Rotterdam, Netherlands.
Elisabeth A M RaevenLaboratory of Medical Immunology, Section Pediatric Infectious Diseases, Department of Laboratory Medicine, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, Netherlands.
Elles R SimonettiLaboratory of Medical Immunology, Section Pediatric Infectious Diseases, Department of Laboratory Medicine, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, Netherlands.
Marc J EleveldLaboratory of Medical Immunology, Section Pediatric Infectious Diseases, Department of Laboratory Medicine, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, Netherlands.
Ronald de GrootLaboratory of Medical Immunology, Section Pediatric Infectious Diseases, Department of Laboratory Medicine, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, Netherlands.
Marien I de JongeLaboratory of Medical Immunology, Section Pediatric Infectious Diseases, Department of Laboratory Medicine, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, Netherlands.
Gerben FerwerdaLaboratory of Medical Immunology, Section Pediatric Infectious Diseases, Department of Laboratory Medicine, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, Netherlands.
Radboud Institute for Molecular Life Sciences · NLRadboud University Medical Center · NLErasmus MC · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type I IFNs, such as interferon alpha and interferon beta, are key regulators of the adaptive immune response during infectious diseases. Type I IFNs are induced upon infection, bind interferon α/β receptors on T-cells and activate intracellular pathways. The activating and inhibitory consequences of type I IFN-signaling are determined by cell type and cellular environment. The neonatal immune system is associated with increased vulnerability to infectious diseases which could partly be explained by an immature CD4

Indexed as

Adaptive ImmunityAdultAge FactorsCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCell ProliferationCells, CulturedCyclin-Dependent Kinase Inhibitor p21Fetal BloodFlow CytometryHumansImmunomagnetic SeparationInfant, NewbornInterferon-betaPrimary Cell CultureReceptor, Interferon alpha-betaCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21IFNAR1 protein, humanIFNAR2 protein, humanInterferon-betaReceptor, Interferon alpha-betaCD4 T cellscell cyclecyclic-dependent kinase inhibitor/p21immunityinterferon betanewbornsproliferationrespiratory syncytial virus

Identifiers

PMID33912177
PMCPMC8071872
OpenAlexW3155887988

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.