Evidence map›Paper›PMID 34724272›Full record

ArticleJournal of the European Academy of Dermatology and Venereology : JEADV2022

Primary alterations during the development of hidradenitis suppurativa.

Z Dajnoki, O Somogyi, B Medgyesi, A Jenei, L Szabó, K Gáspár, Z Hendrik, P Gergely, D Imre, S Póliska and 5 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of the European Academy of Dermatology and Venereology : JEADV, 2022. 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
6.4field-weighted citation impact, top 3% 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, 42 citations in OpenAlex.

  1. Distinct and shared effects of individual γ-secretase inhibitors on human keratinocytes.JID innovations : skin science from molecules to population health · 2026
    Article
  2. Review
  3. Article
  4. Hair follicle stem cell fate supports distinct clinical endotypes in hidradenitis suppurativa.Journal of the European Academy of Dermatology and Venereology : JEADV · 2026
    Article
  5. Review
  6. Review
  7. Hidradenitis Suppurativa Tunnels: Unveiling a Unique Disease Entity.JID innovations : skin science from molecules to population health · 2025
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. A Novel Epidermis Model Using Primary Hidradenitis Suppurativa Keratinocytes.Journal of tissue engineering and regenerative medicine · 2024
    Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. 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

15 authors at 2 institutions in 3 countries.

Z DajnokiDivision of Dermatological Allergology, Department of Dermatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.ORCID https://orcid.org/0000-0002-7787-1002
O SomogyiDivision of Dermatological Allergology, Department of Dermatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
B MedgyesiDivision of Dermatological Allergology, Department of Dermatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
A JeneiDivision of Dermatological Allergology, Department of Dermatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
L SzabóDivision of Dermatological Allergology, Department of Dermatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
K GáspárDivision of Dermatological Allergology, Department of Dermatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Z HendrikDepartment of Forensic Medicine, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
P GergelyDepartment of Forensic Medicine, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
D ImreDepartment of Pathology, Hetényi Géza County Hospital, Szolnok, Hungary.
S PóliskaGenomic Medicine and Bioinformatics Core Facility, Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
D TörőcsikDepartment of Dermatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
C C ZouboulisGenomic Medicine and Bioinformatics Core Facility, Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.ORCID https://orcid.org/0000-0003-1646-2608
E P PrensLaboratory for Experimental Immunodermatology, Erasmus University Medical Center Rotterdam, Rotterdam, Netherlands.
A KapitányDivision of Dermatological Allergology, Department of Dermatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
A SzegediDivision of Dermatological Allergology, Department of Dermatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
University of Debrecen · HUErasmus MC · NL

Funding

EFOP EFOP-3.6.1-16-2016-00022Hungarian Research Grant NKFIH K-128250Hungarian Research Grant NKFIH PD-131689János Bolyai Research Scholarship of the Hungarian Academy of SciencesNew National Excellence Program of the Ministry for Innovation and Technology ÚNKP-20-5
6 · The paper itself

Abstract

backgroundHidradenitis suppurativa (HS) is a chronic, inflammatory disease of the apocrine gland-rich (AGR) skin region. The initial steps of disease development are not fully understood, despite intense investigations into immune alterations in lesional HS skin.

objectivesWe aimed to systematically investigate the inflammatory molecules involved in three stages of HS pathogenesis, including healthy AGR, non-lesional HS and lesional HS skin, with the parallel application of multiple mRNA and protein-based methods.

methodsImmune cell counts (T cells, dendritic cells, macrophages), Th1/Th17-related molecules (IL-12B, TBX21, IFNG, TNFA, IL-17, IL10, IL-23A, TGFB1, RORC, CCL20), keratinocyte-related sensors (TLR2,4), mediators (S100A7, S100A8, S100A9, DEFB4B, LCN2, CAMP, CCL2) and pro-inflammatory molecules (IL1B, IL6, TNFA, IL-23A) were investigated in the three groups by RNASeq, RT-qPCR, immunohistochemistry and immunofluorescence.

resultsEpidermal changes were already detectable in non-lesional HS skin; the epidermal occurrence of antimicrobial peptides (AMPs), IL-1β, TNF-α and IL-23 was highly upregulated compared with healthy AGR skin. In lesional HS epidermis, TNF-α and IL-1β expression remained at high levels while AMPs and IL-23 increased even more compared with non-lesional skin. In the dermis of non-lesional HS skin, signs of inflammation were barely detectable (vs. AGR), while in the lesional dermis, the number of inflammatory cells and Th1/Th17-related mediators were significantly elevated.

conclusionsOur findings that non-lesional HS epidermal keratinocytes produce not only AMPs and IL-1β but also high levels of TNF-α and IL-23 confirm the driver role of keratinocytes in HS pathogenesis and highlight the possible role of keratinocytes in the transformation of non-inflammatory Th17 cells (of healthy AGR skin) into inflammatory cells (of HS) via the production of these mediators. The fact that epidermal TNF-α and IL-23 appear also in non-lesional HS seems to prove these cytokines as excellent therapeutic targets.

Indexed as

Hidradenitis SuppurativaCytokinesEpidermisHumansKeratinocytesSkinCytokines

Identifiers

PMID34724272
PMCPMC9298903
OpenAlexW3208323813

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.