Evidence map›Paper›PMID 32194562›Full record

ArticleFrontiers in immunology2020

Selective Janus Kinase 1 Inhibition Is a Promising Therapeutic Approach for Lupus Erythematosus Skin Lesions.

Tanja Fetter, Paul Smith, Tugce Guel, Christine Braegelmann, Thomas Bieber, Joerg Wenzel

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 2 pooled it
7.7field-weighted citation impact, top 2% 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

37 citing papers in PubMed, 2 syntheses or guidelines pooled it, 60 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. [Lupus erythematosus].Dermatologie (Heidelberg, Germany) · 2025
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. AIM2 and Psoriasis.Frontiers in immunology · 2023
    Review
  18. Review
  19. Treatment of Discoid Lupus Erythematosus with Upadacitinib: A Case Report.Clinical, cosmetic and investigational dermatology · 2023
    Article
  20. Review
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.

Tanja FetterDepartment of Dermatology and Allergy, University Hospital Bonn, Bonn, Germany.
Paul SmithIncyte Corporation, Wilmington, DE, United States.
Tugce GuelDepartment of Dermatology and Allergy, University Hospital Bonn, Bonn, Germany.
Christine BraegelmannDepartment of Dermatology and Allergy, University Hospital Bonn, Bonn, Germany.
Thomas BieberDepartment of Dermatology and Allergy, University Hospital Bonn, Bonn, Germany.
Joerg WenzelDepartment of Dermatology and Allergy, University Hospital Bonn, Bonn, Germany.
University Hospital Bonn · DEIncyte (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Cutaneous lupus erythematosus (CLE) is an interferon (IFN) -driven autoimmune skin disease characterized by an extensive cytotoxic lesional inflammation with activation of different innate immune pathways. Aim of our study was to investigate the specific role of Janus kinase 1 (JAK1) activation in this disease and the potential benefit of selective JAK1 inhibitors as targeted therapy in a preclinical CLE model. Methods: Lesional skin of patients with different CLE subtypes and healthy controls ( Results: Proinflammatory immune pathways, including JAK/STAT signaling, are significantly upregulated within inflamed CLE skin. Here, lesional keratinocytes and dermal immune cells strongly express activated phospho-JAK1. Selective pharmacological JAK1 inhibition significantly reduces the expression of typical proinflammatory mediators such as CXCL chemokines, BLyS, TRAIL, and AIM2 in CLE Conclusion: IFN-associated JAK/STAT activation plays a crucial role in the pathophysiology of CLE. Selective inhibition of JAK1 leads to a decrease of cytokine expression, reduced immune activation, and decline of keratinocyte cell death. Topical treatment with a JAK1-specific inhibitor significantly improves CLE-like skin lesions in a lupus-prone TREX1

Indexed as

AnimalsAzetidinesCell LineCytokinesDisease Models, AnimalDrug Evaluation, PreclinicalEnzyme InductionEnzyme InhibitorsExodeoxyribonucleasesGene Expression RegulationHumansIsonicotinic AcidsJanus Kinase 1KeratinocytesLichen PlanusLupus Erythematosus, CutaneousAzetidinesCytokinesEnzyme InhibitorsExodeoxyribonucleasesINCB039110Isonicotinic AcidsJAK1 protein, humanJak1 protein, mouseJanus Kinase 1Phosphoproteinsthree prime repair exonuclease 1innate immunityinterferonkinase inhibitorlupus erythematosusskin

Identifiers

PMID32194562
PMCPMC7064060
OpenAlexW3009705716

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.