ArticleArthritis & rheumatology (Hoboken, N.J.)2025
Induction of Type I Interferon-Dependent Activation and Migration of Inflammatory Dendritic Cells to Local Lymph Nodes by UV Light Exposure.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
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Who cites it
6 citing papers in PubMed.
- Monocytic niches escape T cell surveillance and promote Mycobacterium tuberculosis persistence in lymph nodes.Immunity · 2026Article
- Single-cell and spatial transcriptomics implicate vascular cell orchestration of inflammatory changes after UV light exposure in skin.The Journal of investigative dermatology · 2026Article
- Dendritic Cell Organization and Function in Innate and Adaptive Immune Defense Within Lymph Nodes.Immunological reviews · 2026Review
- Epidermal Interferon-κ Drives Cutaneous Lupus-Like Lesions, Photosensitivity, and Systemic Autoimmunity In Vivo.Arthritis & rheumatology (Hoboken, N.J.) · 2026Article
- Keratinocyte VISTA attenuates UV light-induced skin injury by suppressing cutaneous type I interferon (IFN-I) response.bioRxiv : the preprint server for biology · 2025Article
- Cutaneous lupus erythematosus - from pathogenesis to targeted therapy.Nature reviews. Rheumatology · 2025Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
objectivePhotosensitivity occurs in ~75% of patients with lupus. Although UV light radiation (UVR) stimulates type I interferon (IFN-I) in the skin, how UVR-induced skin inflammation leads to downstream effects is poorly understood. Tissue inflammation causes dendritic cells (DCs) to migrate from organs to draining lymph nodes (dLN), including a recently identified inflammatory conventional DC subset (inf cDC2) that are potent antigen-presenting cells. To explore links between UVR and the early immune response, we examined DC and lymphocyte subset migration to dLN in normal and lupus-prone mouse strains as well as the role of IFN-I.
methodsMice received a single dose of UV (500 mJ/cm
resultsHigher numbers of CD64+ myeloid cells as well as inf cDC2 were detected in the dLN after UVR in B6 mice, but not in IFN receptor knockout (IFNAR KO) mice. In contrast, Trex1 mutant mice had an exaggerated IFN-I response in the skin and a higher proportion of inf cDC2 in the dLN.
conclusionThese findings reveal a previously unknown relationship between skin UVR and the migration of the inf cDC2 population to dLN. They highlight the role of IFN-I in this process, and the differences between Trex1 mutant and normal mice suggest that this may be of relevance to lupus.
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Registered trials
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