{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T17:29:54Z","timestamp":1773422994194,"version":"3.50.1"},"reference-count":54,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2011,8,1]],"date-time":"2011-08-01T00:00:00Z","timestamp":1312156800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2011,8,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>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\u2212\/\u2212 mice did not increase XPA gene expression and did not enhance the survival of MyD88\u2212\/\u2212-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.<\/jats:p>","DOI":"10.4049\/jimmunol.1100755","type":"journal-article","created":{"date-parts":[[2011,7,16]],"date-time":"2011-07-16T05:09:58Z","timestamp":1310792998000},"page":"1664-1673","source":"Crossref","is-referenced-by-count":22,"title":["Imiquimod-Induced TLR7 Signaling Enhances Repair of DNA Damage Induced by Ultraviolet Light in Bone Marrow-Derived Cells"],"prefix":"10.1093","volume":"187","author":[{"given":"Rita","family":"Fishelevich","sequence":"first","affiliation":[{"name":"Department of Dermatology, School of Medicine, University of Maryland Baltimore , Baltimore, MD 21201"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yuming","family":"Zhao","sequence":"additional","affiliation":[{"name":"Department of Dermatology, School of Medicine, University of Maryland Baltimore , Baltimore, MD 21201"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Papapit","family":"Tuchinda","sequence":"additional","affiliation":[{"name":"Department of Dermatology, School of Medicine, University of Maryland Baltimore , Baltimore, MD 21201"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hannah","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Dermatology, School of Medicine, University of Maryland Baltimore , Baltimore, MD 21201"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ayako","family":"Nakazono","sequence":"additional","affiliation":[{"name":"Department of Dermatology, School of Medicine, University of Maryland Baltimore , Baltimore, MD 21201"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Antonella","family":"Tammaro","sequence":"additional","affiliation":[{"name":"Department of Dermatology, School of Medicine, University of Maryland Baltimore , Baltimore, MD 21201"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tzu-Ching","family":"Meng","sequence":"additional","affiliation":[{"name":"Graceway Pharmaceutical Company , Exton, PA 19341"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jim","family":"Lee","sequence":"additional","affiliation":[{"name":"Graceway Pharmaceutical Company , Exton, PA 19341"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Anthony A","family":"Gaspari","sequence":"additional","affiliation":[{"name":"Department of Dermatology, School of Medicine, University of Maryland Baltimore , Baltimore, MD 21201"},{"name":"Department of Microbiology and Immunology, School of Medicine, University of Maryland Baltimore , Baltimore, MD 21201"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2011,8,15]]},"reference":[{"key":"2025032410284203000_r1","doi-asserted-by":"crossref","first-page":"109","DOI":"10.1007\/978-0-387-78574-5_10","article-title":"Ultraviolet-induced immunosuppression: implications for photocarcinogenesis","volume":"146","author":"Beissert","year":"2009","journal-title":"Cancer Treat. 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