ArticleJournal of immunology (Baltimore, Md. : 1950)2011
Imiquimod-induced TLR7 signaling enhances repair of DNA damage induced by ultraviolet light in bone marrow-derived cells.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 26 citations in OpenAlex.
- Molecular mechanism of Alzheimer's disease using integrated multi-omics.Frontiers in aging neuroscience · 2026Review
- Role of Vitamin C on methotrexate-induced nephrotoxicity in psoriasis context: A preclinical assessment.Toxicology reports · 2024Article
- Irreversible inhibition of estrogen receptor α signaling and the emergence of hormonal resistance in MCF7 breast cancer cells induced by DNA damage agents.Biomedical reports · 2024Article
- Type I Interferons Enhance the Repair of Ultraviolet Radiation-Induced DNA Damage and Regulate Cutaneous Immune Suppression.International journal of molecular sciences · 2022Article
- Nucleic Acid Sensing Pathways in DNA Repair Targeted Cancer Therapy.Frontiers in cell and developmental biology · 2022Review
- Ultraviolet Radiation and Basal Cell Carcinoma: An Environmental Perspective.Frontiers in public health · 2021Review
- Dermatomyositis flare on imiquimod therapy highlights a crucial role of aberrant TLR7 signalling.RMD open · 2016Article
- Ultraviolet radiation signaling through TLR4/MyD88 constrains DNA repair and plays a role in cutaneous immunosuppression.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Indoleamine 2,3-dioxygenase vaccination.Oncoimmunology · 2015Article
- Ultraviolet radiation-induced non-melanoma skin cancer: Regulation of DNA damage repair and inflammation.Genes & diseases · 2014Article
- MyD88 mediates the decision to die by apoptosis or necroptosis after UV irradiation.Innate immunity · 2014Article
- Human in vitro skin organ culture as a model system for evaluating DNA repair.Journal of dermatological science · 2014Article
- Toll-like receptor-4 deficiency enhances repair of UVR-induced cutaneous DNA damage by nucleotide excision repair mechanism.The Journal of investigative dermatology · 2014Article
- Pattern recognition receptors and DNA repair: starting to put a jigsaw puzzle together.Frontiers in immunology · 2014Review
- TLR signaling and DNA repair: are they associated?The Journal of investigative dermatology · 2013Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Imiquimod is a TLR7/8 agonist that has anticancer therapeutic efficacy in the treatment of precancerous skin lesions and certain nonmelanoma skin cancers. To test our hypothesis that imiquimod enhances DNA repair as a mechanism for its anticancer activity, the nucleotide excision repair genes were studied in bone marrow-derived cells. Imiquimod enhanced the expression of xeroderma pigmentosum (XP) A and other DNA repair genes (quantitative real-time PCR analysis) and resulted in an increased nuclear localization of the DNA repair enzyme XPA. This was dependent on MyD88, as bone marrow-derived cells from MyD88(-/-) mice did not increase XPA gene expression and did not enhance the survival of MyD88(-/-)-derived bone marrow-derived cells after UV B exposure as was observed in bone marrow-derived cells from MyD88(+/+) mice. Imiquimod also enhanced DNA repair of UV light (UVL)-irradiated gene expression constructs and accelerated the resolution of cyclobutane pyrimidine dimers after UVL exposures in P388 and XS52. Lastly, topical treatment of mouse skin with 5% imiquimod cream prior to UVL irradiation resulted in a decrease in the number of cyclobutane pyridimine dimer-positive APC that were found in local lymph nodes 24 h after UVL irradiation in both wild-type and IL-12 gene-targeted mice. In total, these data support the idea that TLR7 agonists such as imiquimod enhance DNA repair in bone marrow-derived cells. This property is likely to be an important mechanism for its anticancer effects because it protects cutaneous APC from the deleterious effects of UVL.
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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.