Evidence map›Paper›PMID 35440091›Full record

ArticleCell communication and signaling : CCS2022

Addressing the role of PKD3 in the T cell compartment with knockout mice.

Jiří Koutník, Verena Neururer, Thomas Gruber, Sebastian Peer, Natascha Hermann-Kleiter, William J Olson, Verena Labi, Michael Leitges, Gottfried Baier, Kerstin Siegmund

Open access · goldAbstract readVideo-Audio Media
In one paragraph

Article in Cell communication and signaling : CCS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 46% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. 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 3 institutions in 2 countries.

Jiří KoutníkInstitute of Cell Genetics, Medical University Innsbruck, Innsbruck, Austria.
Verena NeururerInstitute of Cell Genetics, Medical University Innsbruck, Innsbruck, Austria.
Thomas GruberInstitute of Cell Genetics, Medical University Innsbruck, Innsbruck, Austria.
Sebastian PeerInstitute of Cell Genetics, Medical University Innsbruck, Innsbruck, Austria.
Natascha Hermann-KleiterInstitute of Cell Genetics, Medical University Innsbruck, Innsbruck, Austria.
William J OlsonInstitute of Cell Genetics, Medical University Innsbruck, Innsbruck, Austria.
Verena LabiInstitute of Developmental Immunology, Medical University Innsbruck, Innrain 80-82, 6020, Innsbruck, Austria.
Michael LeitgesDivision of BioMedical Sciences, Faculty of Medicine, Craig L Dobbin Genetics Research Centre, Memorial University of Newfoundland Health Science Centre, 300 Prince Philip Drive, St. John's, NF, A1B 3V6, Canada.
Gottfried BaierInstitute of Cell Genetics, Medical University Innsbruck, Innsbruck, Austria.
Kerstin SiegmundInstitute of Cell Genetics, Medical University Innsbruck, Innsbruck, Austria. Kerstin.Siegmund@i-med.ac.at.
Innsbruck Medical University · ATMemorial University of Newfoundland · CAUniversität Innsbruck · AT

Funding

Austrian Science Fund FWF P 31383Austrian Science Fund FWF P 34368Austrian Science Fund FWF TAI 88
6 · The paper itself

Abstract

backgroundThe Protein kinase D3 (PKD3) has been implicated in signal transduction downstream of the T cell receptor (TCR). However, its role for the activation of primary T lymphocytes has not been elucidated so far.

methodsExpression of PKD isoforms in primary murine T cells was determined by RT-PCR and SDS-Page. A germline PKD3-knockout mouse line was analyzed for its immune response to OVA/alum intraperitoneal immunization. Phenotyping of the T cell compartment ex vivo as well as upon stimulation in vitro was performed by flow cytometry. Additionally, cytokine expression was assessed by flow cytometry, RT-PCR and Luminex technology.

resultsPKD expression in T cells is modulated by TCR stimulation, leading to a rapid down-regulation on mRNA and on protein level. PKD3-deficient mice respond to immunization with enhanced T follicular helper cell generation. Furthermore, peripheral PKD3-deficient CD4

conclusionWhile PKD3-deficiency in vivo in mice leads to a skewing of the T cell compartment towards a more activated phenotype, this kinase seems to be dispensable for naïve CD4

Indexed as

T-LymphocytesAnimalsCD4-Positive T-LymphocytesDNA-Activated Protein KinaseDNA-Binding ProteinsMiceMice, KnockoutProtein Kinase CReceptors, Antigen, T-CellDNA-Activated Protein KinaseDNA-Binding ProteinsPrkdc protein, mouseProtein Kinase Cprotein kinase C nuReceptors, Antigen, T-CellPKDProtein kinase DTCR signaling and activationT lymphocyte

Identifiers

PMID35440091
PMCPMC9020081
OpenAlexW4224303931

What Socratic 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 Socratic graph.