Evidence map›Paper›PMID 36466811›Full record

ArticleFrontiers in immunology2022

T cell-intrinsic protein kinase D3 is dispensable for the cells' activation.

Jiří Koutník, Michael Leitges, Kerstin Siegmund

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.1field-weighted citation impact, top 58% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

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

3 authors at 3 institutions in 2 countries.

Jiří KoutníkInstitute of Cell Genetics, Medical University of Innsbruck, Innsbruck, Austria.
Michael LeitgesDivision of BioMedical Sciences, Memorial University of Newfoundland, St. John's, NL, Canada.
Kerstin SiegmundInstitute of Cell Genetics, Medical University of Innsbruck, Innsbruck, Austria.
Innsbruck Medical University · ATMemorial University of Newfoundland · CAUniversität Innsbruck · AT

Funding

Austrian Science Fund FWF P 34368
6 · The paper itself

Abstract

Protein kinases D (PKDs) are implicated in T cell receptor (TCR) signaling. Of the two T cell-expressed isoforms PKD2 and PKD3, however, only the former one is rather well understood in this immune cell type. Recently, we have observed a putative hyper-phenotype of T cells from conventional PKD3-knockout mice, which we explained as a secondary effect due to a skewed T cell compartment from naïve towards effector/memory T cells already under steady state conditions. Nonetheless, to this end it is not clear whether these aberrations are mediated by a T cell-intrinsic or -extrinsic function of PKD3. To address this question, we have investigated mice lacking PKD3 specifically in the T cell compartment. We could show that T cells from CD4-Cre-driven conditional knockout mice did not phenocopy the ones from conventional PKD3-knockout mice. In brief, no skewing in the T cell compartment of peripheral lymphoid organs, no hyper-activation upon stimulation

Indexed as

Germinal CenterReceptors, Antigen, T-CellAnimalsLymphocyte CountMiceMice, KnockoutProtein Kinase CProtein Kinase Cprotein kinase C nuReceptors, Antigen, T-CellLymphatic knockoutProtein kinase D3T cell activationT cell signalingT lymphocyte

Identifiers

PMID36466811
PMCPMC9713823
OpenAlexW4309609027

What OpenQuestion holds

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LicenceCC BY
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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.