ArticleArthritis & rheumatology (Hoboken, N.J.)2017
Ultraviolet B Irradiation Causes Stimulator of Interferon Genes-Dependent Production of Protective Type I Interferon in Mouse Skin by Recruited Inflammatory Monocytes.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 75 citations in OpenAlex.
- Endothelial cell expression of STINGThe Journal of investigative dermatology · 2026Article
- Keratinocytes: A key player in skin immunity and their emerging roles in secondary lymphedema.JID innovations : skin science from molecules to population health · 2026Review
- Mucosal-associated invariant T cells support IL-15-dependent Treg response in skin injury and promote resolution of skin inflammation.bioRxiv : the preprint server for biology · 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
- Integrative Analyses Identify a cGAS-STING Pathway-Driven Signature With Context-Dependent Roles in Systemic Lupus Erythematosus.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Loss of Tripartite Motif-Containing Protein 21 and UVB-Induced Systemic Inflammation by Regulating DNA-Sensing Pathways.Arthritis & rheumatology (Hoboken, N.J.) · 2026Article
- Epigenetic reprogramming in autoimmune and immune-mediated skin disease.Frontiers in immunology · 2026Review
- Immunopathogenesis and Therapeutics of Systemic Lupus Erythematosus: an Integrative Review.Clinical reviews in allergy & immunology · 2025Review
- Induction of Type I Interferon-Dependent Activation and Migration of Inflammatory Dendritic Cells to Local Lymph Nodes by UV Light Exposure.Arthritis & rheumatology (Hoboken, N.J.) · 2025Article
- Photoaging: UV radiation-induced cGAS-STING signaling promotes the aging process in skin by remodeling the immune network.Biogerontology · 2025Review
- Systemic lupus erythematosus: updated insights on the pathogenesis, diagnosis, prevention and therapeutics.Signal transduction and targeted therapy · 2025Review
- Focus on Interferon Signature in Cutaneous Lupus Erythematosus: Novel Therapies From Better Understanding of the Pathogenesis.Journal of immunology research · 2025Review
- C/EBPβ Deficiency Enhances Keratinocyte Apoptosis after UVB-Induced DNA Damage via Regulation of the Type I IFN and TNF Responses.Frontiers in cell death · 2025Article
- Understanding the Role of Type I Interferons in Cutaneous Lupus and Dermatomyositis: Toward Better Therapeutics.Arthritis & rheumatology (Hoboken, N.J.) · 2025Review
- Lupus-prone NZM2328 mice exhibit enhanced UV-induced myeloid cell recruitment and activation in a type I interferon dependent manner.Journal of autoimmunity · 2024Article
- Article
- Crosslinking of Ly6a metabolically reprograms CD8 T cells for cancer immunotherapy.Nature communications · 2024Article
- Monocyte infiltration is an independent positive prognostic biomarker in vulvar squamous cell carcinoma.Cancer immunology, immunotherapy : CII · 2024Article
- The interferon-rich skin environment regulates Langerhans cell ADAM17 to promote photosensitivity in lupus.eLife · 2024Article
- Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
objectivePhotosensitivity is common in patients with systemic lupus erythematosus, although the mechanisms linking ultraviolet (UV) light to flares are not well understood. We undertook this study to determine whether repetitive UVB exposure could induce type I interferon (IFN) production in normal mouse skin, and to investigate the roles of inflammatory monocytes and plasmacytoid dendritic cells (PDCs) in type I IFN production and development of UVB irradiation-induced inflammation.
methodsMice were irradiated with UVB at 100 mJ/cm
resultsRepeated UVB irradiation stimulated an inflammatory cell infiltrate and induction of type I IFN and proinflammatory cytokines. Interestingly, the type I IFN response was independent of PDCs but dependent on inflammatory monocytes, which were recruited following UVB irradiation. The adaptor protein STING was necessary for both type I IFN and proinflammatory cytokine expression in the skin. UVB-irradiated IFNAR-knockout mice showed increased levels of proinflammatory genes and more severe inflammation by histology, suggesting a protective role for type I IFN.
conclusionIn wild-type mice, repeated doses of UVB irradiation induce monocyte-dependent and PDC-independent expression of type I IFN together with expression of other proinflammatory cytokines. Induction is dependent on the adaptor protein STING. Surprisingly, studies using IFNAR-deficient mice revealed that type I IFN protects against UVB irradiation-induced skin inflammation, in part by attenuating proinflammatory cytokine expression and limiting tissue damage.
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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.