ArticleThe Journal of investigative dermatology2014
UVB-induced skin inflammation and cutaneous tissue injury is dependent on the MHC class I-like protein, CD1d.
Article in The Journal of investigative dermatology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 47 citations in OpenAlex.
- Supercritical COMaterials today. Bio · 2026Article
- Targeting β2-adrenergic receptor reduces UV-induced cutaneous damage and inflammation in a murine model.Journal of photochemistry and photobiology · 2025Article
- ZBP1-mediated PANoptosis is a crucial lethal form in diverse keratinocyte death modalities in UVB-induced skin injury.Cell death & disease · 2025Article
- From neglect to necessity: the role of innate immunity in cutaneous squamous cell carcinoma therapy.Frontiers in immunology · 2025Review
- ZnO Nanoparticles as Potent Inducers of Dermal Immunosuppression in Contact Hypersensitivity in Mice.ACS nano · 2024Article
- Aloe Extracts Inhibit Skin Inflammatory Responses by Regulating NF-κB, ERK, and JNK Signaling Pathways in an LPS-Induced RAW264.7 Macrophages Model.Clinical, cosmetic and investigational dermatology · 2023Article
- Fibroblast growth factor 10 protects against UVB-induced skin injury by activating the ERK/YAP signalling pathway.Cell proliferation · 2022Article
- Protective Function ofPlants (Basel, Switzerland) · 2022Article
- Jelly Fig (Antioxidants (Basel, Switzerland) · 2022Article
- Roles and therapeutic potential of CD1d-Restricted NKT cells in inflammatory skin diseases.Frontiers in immunology · 2022Review
- Topically Applied Taurine Chloramine Protects against UVB-Induced Oxidative Stress and Inflammation in Mouse Skin.Antioxidants (Basel, Switzerland) · 2021Article
- Influence of3 Biotech · 2021Article
- Radiofrequency Irradiation Attenuates High-Mobility Group Box 1 and Toll-like Receptor Activation in Ultraviolet B-Induced Skin Inflammation.Molecules (Basel, Switzerland) · 2021Article
- Application of adipose-derived stem cells in photoaging: basic science and literature review.Stem cell research & therapy · 2020Review
- Article
- The Role of the Immune System in Cutaneous Squamous Cell Carcinoma.International journal of molecular sciences · 2019Review
- Long non-coding RNA HOTAIR promotes UVB-induced apoptosis and inflammatory injury by up-regulation of PKR in keratinocytes.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2018Article
- Article
- Role of p53 in silibinin-mediated inhibition of ultraviolet B radiation-induced DNA damage, inflammation and skin carcinogenesis.Carcinogenesis · 2017Article
- The photoprotective effects of 2-benzoyl-3-phenylquinoxaline 1,4-dioxide against UVB-induced damage in HaCaT cells.Medical oncology (Northwood, London, England) · 2016Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CD1d is a major histocompatibility complex class 1-like molecule that regulates the function and development of natural killer T (NKT) cells. Previously, we identified a critical role for the CD1d-NKT cell arm of innate immunity in promoting the development of UVB-induced p53 mutations, immune suppression, and skin tumors. Sunburn, an acute inflammatory response to UVB-induced cutaneous tissue injury, represents a clinical marker for non-melanoma skin cancer (NMSC) risk. However, the innate immune mechanisms controlling sunburn development are not considered relevant in NMSC etiology, and remain poorly investigated. Here we found that CD1d knockout (CD1d(-/-)) mice resist UVB-induced cutaneous tissue injury and inflammation compared with wild-type (WT) mice. This resistance was coupled with a faster epithelial tissue healing response. In contrast, the skins of UVB-irradiated invariant NKT cell-knockout (Jα18(-/-)) and NKT cell-deficient (TCRα(-/-)) mice, which express CD1d but are deficient in CD1d-dependent NKT cells, exhibited as much cutaneous tissue injury and inflammation as WT mice. In the absence of NKT cells, CD1d-deficient keratinocytes, dendritic cells, and macrophages exhibited diminished basal and stress-induced levels of pro-inflammatory mediators. Thus, our findings identify an essential role for CD1d in promoting UVB-induced cutaneous tissue injury and inflammation. They also suggest sunburn and NMSC etiologies are immunologically linked.
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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.