Evidence map›Paper›PMID 26288353›Full record

ArticleThe Journal of investigative dermatology2015

IFNλ Stimulates MxA Production in Human Dermal Fibroblasts via a MAPK-Dependent STAT1-Independent Mechanism.

Adewonuola A Alase, Yasser M El-Sherbiny, Edward M Vital, Desmond J Tobin, Neil A Turner, Miriam Wittmann

Abstract read
PubMed Publisher
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 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

20 citing papers in PubMed, 25 citations in OpenAlex.

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  11. Interferons: Tug of War Between Bacteria and Their Host.Frontiers in cellular and infection microbiology · 2021
    Review
  12. Review
  13. Review
  14. Differential Regulation of Type I and Type III Interferon Signaling.International journal of molecular sciences · 2019
    Review
  15. Review
  16. Review
  17. Article
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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

6 authors at 2 institutions in 2 countries.

Adewonuola A AlaseCentre for Skin Sciences, Faculty of Life Sciences, University of Bradford, Bradford, UK. Electronic address: a.a.alase@student.bradford.ac.uk.
Yasser M El-SherbinyLeeds Institute of Rheumatic and Musculoskeletal Medicine (LIRMM), Faculty of Medicine and Health, University of Leeds, Leeds, UK; Clinical Pathology Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt.
Edward M VitalLeeds Institute of Rheumatic and Musculoskeletal Medicine (LIRMM), Faculty of Medicine and Health, University of Leeds, Leeds, UK.
Desmond J TobinCentre for Skin Sciences, Faculty of Life Sciences, University of Bradford, Bradford, UK.
Neil A TurnerDivision of Cardiovascular and Diabetes Research, Leeds Institute for Cardiovascular and Diabetes Research (LICAMM), Faculty of Medicine and Health, University of Leeds, Leeds, UK.
Miriam WittmannCentre for Skin Sciences, Faculty of Life Sciences, University of Bradford, Bradford, UK; Leeds Institute of Rheumatic and Musculoskeletal Medicine (LIRMM), Faculty of Medicine and Health, University of Leeds, Leeds, UK; Department of Dermatology, Bradford Teaching Hospitals NHS Foundation Trust, St Luke's Hospital, Bradford, UK; Leeds Musculoskeletal Biomedical Research Unit, National Institute of Health Research (NIHR), Chapel Allerton Hospital, Leeds, UK.
University of Leeds · GBUniversity of Bradford · GB

Funding

Department of Health CS-2013-13-032
6 · The paper itself

Abstract

IFNλ is important for epidermal defense against viruses. It is produced by, and acts on, keratinocytes, whereas fibroblasts were previously considered to be unresponsive to this type III IFN. Herein we report findings revealing cell type-specific differences in IFNλ signaling and function in skin resident cells. In dermal fibroblasts, IFNλ induced the expression of myxovirus protein A (MxA), a potent antiviral factor, but not other IFN signature genes as it does in primary keratinocytes. In contrast to its effect on keratinocytes, IFNλ did not phosphorylate signal transducer and activator of transcription 1 in fibroblasts, but instead activated mitogen activated protein kinases (MAPK). Accordingly, inhibition of MAPK activation (p38 and p42/44) blocked the expression of MxA protein in fibroblasts but not in keratinocytes. Functionally, IFNλ inhibited proliferation in keratinocytes but not in fibroblasts. Moreover, IFNλ upregulated the expression of Tumor growth factor beta 1 (TGFβ1)-induced collagens in fibroblasts. Taken together, our findings identify primary human dermal fibroblasts as responder cells to IFNλ. Our study shows cutaneous cell type-specific IFN signaling and suggests that IFNλ, although important for epidermal antiviral competence, may also have a regulatory role in the dermal compartment balancing type I IFN-induced inhibition of tissue repair processes.

Indexed as

Cells, CulturedFibroblastsHumansInterferon-alphaInterferon-gammaInterferon gamma ReceptorMitogen-Activated Protein KinasesMyxovirus Resistance ProteinsReceptors, InterferonSkinSTAT1 Transcription FactorTransforming Growth Factor beta1Interferon-alphaInterferon-gammaInterferon gamma ReceptorMitogen-Activated Protein KinasesMX1 protein, humanMyxovirus Resistance ProteinsReceptors, InterferonSTAT1 protein, humanSTAT1 Transcription FactorTransforming Growth Factor beta1

Identifiers

PMID26288353
OpenAlexW1937191153

What OpenQuestion holds

Textmetadata
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.