ArticleArthritis & rheumatology (Hoboken, N.J.)2026
Epidermal Interferon-κ Drives Cutaneous Lupus-Like Lesions, Photosensitivity, and Systemic Autoimmunity In Vivo.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Endothelial cell expression of STINGThe Journal of investigative dermatology · 2026Article
- Cutaneous lupus erythematosus - from pathogenesis to targeted therapy.Nature reviews. Rheumatology · 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
15 authors.
Funding
Abstract
objectiveKeratinocyte-derived interferon (IFN) κ is chronically overexpressed in human nonlesional systemic lupus erythematosus (SLE) skin. Recent evidence suggests that epidermal signals instruct the immune system in SLE, but whether epidermal IFNκ alone is sufficient to drive lupus phenotypes has not been investigated. This study aimed to identify whether epidermal-specific overexpression of IFN-κ (Ifnk) results in lupus-like cutaneous and systemic inflammation.
methodsWe compared 3-month-old (young) and 12-month-old (aged) Balb/c mice who overexpress Ifnk in the epidermis under the keratin 14 promoter (transgenic [TG]) with age-matched Balb/c wild-type mice and assessed local and systemic immune responses at baseline and after UV treatment. Skin lesions were assessed by histopathology, bulk RNA sequencing, and immunohistochemistry and subsequently compared to human cutaneous lupus erythematosus (CLE). Flow cytometry on lymph nodes and splenocytes at baseline and after UV treatment was performed to phenotype immune cell compositions.
resultsIfnk TG mice spontaneously developed CLE-like lesions and systemic immune dysregulation. Lesions showed facial predominance, lymphocytic infiltration, immune complex deposition, and a transcriptional signature reflective of human CLE. Ifnk TG mice exhibited increased immune cell activation and spontaneous signs of systemic autoimmunity with higher anti-double-stranded DNA antibodies, lymphadenopathy, and splenomegaly but lacked signs of renal inflammation. UV treatment enhanced cutaneous inflammation and splenic T cell activation in Ifnk TG mice.
conclusionTogether, we describe a new CLE mouse model that recapitulates features of human CLE and substantiates the role of epidermal IFNκ as a driver of CLE, photosensitivity, and systemic inflammation.
Indexed as
Identifiers
What Socratic 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 Socratic graph.