ReviewJournal of immunology research2025
Focus on Interferon Signature in Cutaneous Lupus Erythematosus: Novel Therapies From Better Understanding of the Pathogenesis.
Review in Journal of immunology research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
- Focus on Interferon Signature in Cutaneous Lupus Erythematosus: Novel Therapies From Better Understanding of the Pathogenesis.Journal of immunology research · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cutaneous lupus erythematosus (CLE), a common clinical manifestation of lupus erythematosus (LE), significantly compromises patients' quality of life and social functioning due to its relatively high prevalence. While the exact pathogenesis of CLE remains incompletely understood, accumulating evidence highlights the pivotal role of interferon (IFN) as a central mediator in disease initiation and progression. Stromal cells and infiltrating immune cells within CLE lesions demonstrate elevated expression of IFN-stimulated genes (ISGs), establishing a characteristic IFN signature. IFN orchestrates multiple pathological processes, including chemokine-mediated immune cell recruitment, cutaneous inflammation cascade, and tissue fibrosis. This review systematically examines the IFN-CLE axis through an integrated analysis of in vitro and in vivo experimental data. Emerging clinical trials reveal therapeutic promise in strategies targeting plasmacytoid dendritic cells (pDCs), neutralizing IFN signaling, or blocking downstream pathways. Given the current limitations in CLE management, IFN-focused strategies may offer innovative solutions to address unmet clinical needs through precision immunomodulation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.