Evidence map›Paper›PMID 37140884›Full record

ReviewAmerican journal of clinical dermatology2023

Cutaneous Lupus Erythematosus: An Update on Pathogenesis and Future Therapeutic Directions.

Dennis Niebel, Luka de Vos, Tanja Fetter, Christine Brägelmann, Jörg Wenzel

Open access · hybridAbstract readReview
In one paragraph

Review in American journal of clinical dermatology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
18.2field-weighted citation impact, top 1% 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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.

  1. Pooled it
  2. Litifilimab efficacy on skin outcomes in cutaneous lupus erythematosus in the Phase 2 LILAC study.Journal of the European Academy of Dermatology and Venereology : JEADV · 2026
    Trial
  3. Trial
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Keratinocytes: A key player in skin immunity and their emerging roles in secondary lymphedema.JID innovations : skin science from molecules to population health · 2026
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. [Chronic scarring plaques: a leap forward in treatment].Dermatologie (Heidelberg, Germany) · 2026
    Article
  19. Review
  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

5 authors at 2 institutions in 1 country.

Dennis Niebel *Department of Dermatology, University Hospital Regensburg, 93053, Regensburg, Germany.ORCID http://orcid.org/0000-0003-2069-0486
Luka de Vos *Department of Dermatology, University Hospital Bonn, 53127, Bonn, Germany.
Tanja FetterDepartment of Dermatology, University Hospital Bonn, 53127, Bonn, Germany.
Christine BrägelmannDepartment of Dermatology, University Hospital Bonn, 53127, Bonn, Germany.ORCID http://orcid.org/0000-0002-0496-9041
Jörg WenzelDepartment of Dermatology, University Hospital Bonn, 53127, Bonn, Germany. Joerg.Wenzel@ukbonn.de.ORCID http://orcid.org/0000-0002-4744-5993
University Hospital Bonn · DEUniversity Hospital Regensburg · DE

Funding

Medizinische Fakultät, Rheinische Friedrich-Wilhelms-Universität Bonn grant 2022-1A-08
6 · The paper itself

Abstract

Lupus erythematosus comprises a spectrum of autoimmune diseases that may affect various organs (systemic lupus erythematosus [SLE]) or the skin only (cutaneous lupus erythematosus [CLE]). Typical combinations of clinical, histological and serological findings define clinical subtypes of CLE, yet there is high interindividual variation. Skin lesions arise in the course of triggers such as ultraviolet (UV) light exposure, smoking or drugs; keratinocytes, cytotoxic T cells and plasmacytoid dendritic cells (pDCs) establish a self-perpetuating interplay between the innate and adaptive immune system that is pivotal for the pathogenesis of CLE. Therefore, treatment relies on avoidance of triggers and UV protection, topical therapies (glucocorticosteroids, calcineurin inhibitors) and rather unspecific immunosuppressive or immunomodulatory drugs. Yet, the advent of licensed targeted therapies for SLE might also open new perspectives in the management of CLE. The heterogeneity of CLE might be attributable to individual variables and we speculate that the prevailing inflammatory signature defined by either T cells, B cells, pDCs, a strong lesional type I interferon (IFN) response, or combinations of the above might be suitable to predict therapeutic response to targeted treatment. Therefore, pretherapeutic histological assessment of the inflammatory infiltrate could stratify patients with refractory CLE for T-cell-directed therapies (e.g. dapirolizumab pegol), B-cell-directed therapies (e.g. belimumab), pDC-directed therapies (e.g. litifilimab) or IFN-directed therapies (e.g. anifrolumab). Moreover, Janus kinase (JAK) and spleen tyrosine kinase (SYK) inhibitors might broaden the therapeutic armamentarium in the near future. A close interdisciplinary exchange with rheumatologists and nephrologists is mandatory for optimal treatment of lupus patients to define the best therapeutic strategy.

Indexed as

Lupus Erythematosus, CutaneousLupus Erythematosus, SystemicHumansImmunosuppressive AgentsKeratinocytesSkinImmunosuppressive Agents

Identifiers

PMID37140884
PMCPMC10157137
OpenAlexW4368360652

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.