Evidence map›Paper›PMID 25078666›Full record

ArticleThe Journal of investigative dermatology2015

The late endosomal adaptor molecule p14 (LAMTOR2) regulates TGFβ1-mediated homeostasis of Langerhans cells.

Florian Sparber, Christoph H Tripp, Kerstin Komenda, Julia M Scheffler, Björn E Clausen, Lukas A Huber, Nikolaus Romani, Patrizia Stoitzner

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of investigative dermatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 27 citations in OpenAlex.

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  15. Langerhans cell origin and regulation.Current opinion in hematology · 2016
    Review
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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 2 institutions in 2 countries.

Florian SparberDepartment of Dermatology and Venereology, Innsbruck Medical University, Innsbruck, Austria.
Christoph H TrippDepartment of Dermatology and Venereology, Innsbruck Medical University, Innsbruck, Austria.
Kerstin KomendaDepartment of Dermatology and Venereology, Innsbruck Medical University, Innsbruck, Austria.
Julia M SchefflerDivision of Cell Biology, Biocenter Innsbruck, Innsbruck, Austria.
Björn E ClausenInstitute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.
Lukas A HuberDivision of Cell Biology, Biocenter Innsbruck, Innsbruck, Austria.
Nikolaus RomaniDepartment of Dermatology and Venereology, Innsbruck Medical University, Innsbruck, Austria.
Patrizia StoitznerDepartment of Dermatology and Venereology, Innsbruck Medical University, Innsbruck, Austria. Electronic address: patrizia.stoitzner@i-med.ac.at.
Innsbruck Medical University · ATJohannes Gutenberg University Mainz · DE

Funding

Austrian Science Fund FWF P 21487Austrian Science Fund FWF P 23548
6 · The paper itself

Abstract

Langerhans cells (LCs), a sub-population of dendritic cells (DCs) in the skin, participate in the regulation of immunity and peripheral tolerance. The adaptor molecule p14 is part of the late endosomal/lysosomal adaptor and mitogen-activated protein kinase and mammalian target of rapamycin (mTOR) activator/regulator (LAMTOR) complex, which mediates the activation of lysosome-associated extracellular signaling-regulated kinase (ERK) and the mTOR cascade. In previous work, we demonstrated that CD11c-specific deficiency of p14 disrupts LC homeostasis by affecting the LAMTOR-mediated ERK and mTOR signaling. In this study, we extended our analysis on p14 deficiency specifically in LCs. Langerin-specific ablation of p14 caused a complete loss of LCs, accompanied by an increased maturational phenotype of LCs. The absence of LCs in p14-deficient mice reduced contact hypersensitivity (CHS) responses to the contact sensitizer trinitrochlorobenzene. Analysis using bone marrow-derived DCs (BMDCs) revealed that p14 deficiency in DCs/LCs interfered with the LC-relevant transforming growth factor β1 (TGFβ1) pathway, by lowering TGFβ receptor II expression on BMDCs and LCs, as well as surface binding of TGFβ1 on BMDCs. We conclude that p14 deficiency affects TGFβ1 sensitivity of LCs, which is mandatory for their homeostasis and subsequently for their immunological function during CHS.

Indexed as

AnimalsCD11c AntigenCell MovementDermatitis, ContactDown-RegulationEndosomesFemaleHomeostasisImmune ToleranceImmunophenotypingLangerhans CellsMaleMAP Kinase Signaling SystemMice, Mutant StrainsProteinsProtein Serine-Threonine KinasesCD11c AntigenLAMTOR2 protein, mouseProteinsProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IReceptor, Transforming Growth Factor-beta Type IITgfb1 protein, mouseTransforming Growth Factor beta1

Identifiers

PMID25078666
PMCPMC4285575
OpenAlexW2137577162

What OpenQuestion holds

Textmetadata
LicenceTDM
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.