Evidence map›Paper›PMID 38510961›Full record

ArticleFrontiers in cellular and infection microbiology2024

The cutaneous beta human papillomavirus type 8 E6 protein induces CCL2 through the CEBPα/miR-203/p63 pathway to support an inflammatory microenvironment in epidermodysplasia verruciformis skin lesions.

Luca Vella, Anna Sternjakob, Stefan Lohse, Alina Fingerle, Tanya Sperling, Claudia Wickenhauser, Michael Stöckle, Thomas Vogt, Klaus Roemer, Monika Ołdak and 1 more

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

Article in Frontiers in cellular and infection microbiology, 2024. 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
–field-weighted citation impact, top 97% 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, 0 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

11 authors at 4 institutions in 2 countries.

Luca VellaInstitute of Virology, Saarland University Medical Center, Homburg, Germany.
Anna SternjakobInstitute of Virology, Saarland University Medical Center, Homburg, Germany.
Stefan LohseInstitute of Virology, Saarland University Medical Center, Homburg, Germany.
Alina FingerleInstitute of Virology, Saarland University Medical Center, Homburg, Germany.
Tanya SperlingInstitute of Virology, University of Cologne, Cologne, Germany.
Claudia WickenhauserInstitute of Pathology, University of Cologne, Cologne, Germany.
Michael StöckleDepartment of Urology and Pediatric Urology, Saarland University Medical Center, Homburg, Germany.
Thomas VogtDepartment of Dermatology, Saarland University Medical Center, Homburg, Germany.
Klaus RoemerJose Carreras Center for Immune and Gene Therapy, Saarland University Medical Center, Homburg, Germany.
Monika OłdakInstitute of Virology, Saarland University Medical Center, Homburg, Germany.
Sigrun SmolaInstitute of Virology, Saarland University Medical Center, Homburg, Germany.
Saarland University · DEUniversity of Cologne · DEHelmholtz Centre for Infection Research · DEMedical University of Warsaw · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human papillomavirus type 8 (HPV8), a cutaneous genus beta HPV type, has co-carcinogenic potential at sun-exposed sites in patients suffering from the inherited skin disease epidermodysplasia verruciformis (EV). We had previously shown that Langerhans cells responsible for epithelial immunosurveillance were strongly reduced at infected sites and that the HPV8 E7 protein interferes with the CCAAT/enhancer-binding protein (C/EBP)β to suppress the Langerhans cell chemokine CCL20. At the same time, however, we observed that EV lesions are heavily infiltrated with inflammatory immune cells, which is similar to the situation in HPV8 E6 transgenic mice. To identify critical inflammatory factors, we used a broad multiplex approach and found that the monocyte attracting chemokine CCL2 was significantly and strongly induced by HPV8 E6 but not E7-expressing HaCaT cells, which were used as a model for UV-damaged skin keratinocytes. Conditioned media from HPV8 E6-expressing keratinocytes enhanced CCL2-receptor (CCR2)-dependent monocyte recruitment

Indexed as

Chemokine CCL2Epidermodysplasia VerruciformisMicroRNAsAnimalsHuman Papillomavirus VirusesHumansKeratinocytesMiceMice, TransgenicTumor Necrosis Factor-alphaCCL2 protein, humanCcl2 protein, mouseChemokine CCL2MicroRNAsMIRN203 microRNA, humanTumor Necrosis Factor-alphaCCL2C/EBPE6epidermodysplasia verruciformisHPVinflammationmacrophagep63

Identifiers

PMID38510961
PMCPMC10953690
OpenAlexW4392507048

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.