ArticleThe Journal of investigative dermatology2014
Toll-like receptor-4 deficiency enhances repair of UVR-induced cutaneous DNA damage by nucleotide excision repair mechanism.
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 21 papers.
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Who cites it
21 citing papers in PubMed, 44 citations in OpenAlex.
- MyD88 Plays an Important Role in UVB-Induced Suppression of Dendritic Cell Activity, T Cell Function, and Cutaneous Immune Response.International journal of molecular sciences · 2025Article
- An immunomodulating peptide to counteract solar radiation-induced immunosuppression and DNA damage.Scientific reports · 2023Article
- Effects of donkey milk on UVB-induced skin barrier damage and melanin pigmentation: A network pharmacology and experimental validation study.Frontiers in nutrition · 2023Article
- Type I Interferons Enhance the Repair of Ultraviolet Radiation-Induced DNA Damage and Regulate Cutaneous Immune Suppression.International journal of molecular sciences · 2022Article
- Article
- TLR4 gene polymorphisms in Egyptian vitiligo patients: insights into emerging association with clinical activity, family history, and response to therapy.Journal, genetic engineering & biotechnology · 2021Article
- From Merkel Cell Polyomavirus Infection to Merkel Cell Carcinoma Oncogenesis.Frontiers in microbiology · 2021Review
- Photoimmunology: how ultraviolet radiation affects the immune system.Nature reviews. Immunology · 2019Review
- TLR4 in skin cancer: From molecular mechanisms to clinical interventions.Molecular carcinogenesis · 2019Article
- Protective Effect of Baicalin Against TLR4-mediated UVA-induced Skin Inflammation.Photochemistry and photobiology · 2019Article
- Loss of INK4a/Arf gene enhances ultraviolet radiation-induced cutaneous tumor development.Experimental dermatology · 2017Article
- Evidence for biochemical barrier restoration: Topical solenopsin analogs improve inflammation and acanthosis in the KC-Tie2 mouse model of psoriasis.Scientific reports · 2017Article
- Genetic Variability as a Regulator of TLR4 and NOD Signaling in Response to Bacterial Driven DNA Damage Response (DDR) and Inflammation: Focus on the Gastrointestinal (GI) Tract.Frontiers in genetics · 2017Review
- Baicalin Protects Keratinocytes from Toll-like Receptor-4 Mediated DNA Damage and Inflammation Following Ultraviolet Irradiation.Photochemistry and photobiology · 2015Article
- Ultraviolet radiation-induced non-melanoma skin cancer: Regulation of DNA damage repair and inflammation.Genes & diseases · 2014Article
- UVB radiation illuminates the role of TLR3 in the epidermis.The Journal of investigative dermatology · 2014Review
- Skin cancer in organ transplant recipients: more than the immune system.Journal of the American Academy of Dermatology · 2014Review
- Photoimmunology.Dermatologic clinics · 2014Review
- Innate immune sensors stimulate inflammatory and immunosuppressive responses to UVB radiation.The Journal of investigative dermatology · 2014Article
- Pattern recognition receptors and DNA repair: starting to put a jigsaw puzzle together.Frontiers in immunology · 2014Review
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10 authors at 1 institution in 1 country.
Funding
Abstract
UVB-induced DNA damage has a critical role in the development of photoimmunosuppression. The purpose of this study was to determine whether repair of UVB-induced DNA damage is regulated by Toll-like receptor-4 (TLR4). When TLR4 gene knockout (TLR4(-/-)) and TLR4-competent (TLR4(+/+)) mice were subjected to 90 mJ cm(-2) UVB radiation locally, DNA damage in the form of cyclobutane pyrimidine dimers (CPDs) was repaired more efficiently in the skin and bone marrow-derived dendritic cells (BMDCs) of TLR4(-/-) mice in comparison to TLR4(+/+) mice. Expression of DNA repair gene XPA (xeroderma pigmentosum complementation group A) was significantly lower in skin and BMDCs of TLR4(+/+) mice than TLR4(-/-) mice after UVB exposure. When cytokine levels were compared in these strains after UVB exposure, BMDCs from UV-irradiated TLR4(-/-) mice produced significantly more interleukin (IL)-12 and IL-23 cytokines (P<0.05) than BMDCs from TLR4(+/+) mice. Addition of anti-IL-12 and anti-IL-23 antibodies to BMDCs of TLR4(-/-) mice (before UVB exposure) inhibited repair of CPDs, with a concomitant decrease in XPA expression. Addition of TLR4 agonist to TLR4(+/+) BMDC cultures decreased XPA expression and inhibited CPD repair. Thus, strategies to inhibit TLR4 may allow for immunopreventive and immunotherapeutic approaches for managing UVB-induced cutaneous DNA damage and skin cancer.
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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.