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• W2014026197 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 90mJcm−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. 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 90mJcm−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." @default.
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• W2014026197 date "2014-06-01" @default.
• W2014026197 modified "2023-10-15" @default.
• W2014026197 title "Toll-Like Receptor-4 Deficiency Enhances Repair of UVR-Induced Cutaneous DNA Damage by Nucleotide Excision Repair Mechanism" @default.
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• W2014026197 doi "https://doi.org/10.1038/jid.2013.530" @default.
• W2014026197 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4020975" @default.
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