{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T02:19:45Z","timestamp":1791944385685,"version":"4.3.4"},"reference-count":50,"publisher":"Oxford University Press (OUP)","issue":"5","license":[{"start":{"date-parts":[[2014,9,1]],"date-time":"2014-09-01T00:00:00Z","timestamp":1409529600000},"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":[[2014,9,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Persistent infection with high-risk human papillomaviruses (HPV) causes epithelial hyperplasia that can progress to cancer and is thought to depend on immunosuppressive mechanisms that prevent viral clearance by the host. IL-17 is a cytokine with diverse functions in host defense and in the pathology of autoimmune disorders, chronic inflammatory diseases, and cancer. We analyzed biopsies from patients with HPV-associated cervical intraepithelial neoplasia grade 2\/3 and murine skin displaying HPV16 E7 protein-induced epithelial hyperplasia, which closely models hyperplasia in chronic HPV lesions. Expression of IL-17 and IL-23, a major inducer of IL-17, was elevated in both human HPV-infected and murine E7-expressing lesions. Using a skin-grafting model, we demonstrated that IL-17 in HPV16 E7 transgenic skin grafts inhibited effective host immune responses against the graft. IL-17 was produced by CD3+ T cells, predominantly CD4+ T cells in human, and CD4+ and \u03b3\u03b4 T cells in mouse hyperplastic lesions. IL-23 and IL-1\u03b2, but not IL-18, induced IL-17 production in E7 transgenic skin. Together, these findings demonstrate an immunosuppressive role for IL-17 in HPV-associated epithelial hyperplasia and suggest that blocking IL-17 in persistent viral infection may promote antiviral immunity and prevent progression to cancer.<\/jats:p>","DOI":"10.4049\/jimmunol.1400216","type":"journal-article","created":{"date-parts":[[2014,7,26]],"date-time":"2014-07-26T03:41:37Z","timestamp":1406346097000},"page":"2248-2257","source":"Crossref","is-referenced-by-count":72,"title":["IL-17 Suppresses Immune Effector Functions in Human Papillomavirus-Associated Epithelial Hyperplasia"],"prefix":"10.1093","volume":"193","author":[{"given":"Christina","family":"Gosmann","sequence":"first","affiliation":[{"name":"University of Queensland Diamantina Institute, Translational Research Institute , Brisbane, Queensland 4102 ,","place":["Australia"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephen R","family":"Mattarollo","sequence":"additional","affiliation":[{"name":"University of Queensland Diamantina Institute, Translational Research Institute , Brisbane, Queensland 4102 ,","place":["Australia"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jennifer A","family":"Bridge","sequence":"additional","affiliation":[{"name":"University of Queensland Diamantina Institute, Translational Research Institute , Brisbane, Queensland 4102 ,","place":["Australia"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ian H","family":"Frazer","sequence":"additional","affiliation":[{"name":"University of Queensland Diamantina Institute, Translational Research Institute , Brisbane, Queensland 4102 ,","place":["Australia"]},{"name":"Australian Infectious Diseases Research Centre, University of Queensland , Brisbane, Queensland 4102 ,","place":["Australia"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Antje","family":"Blumenthal","sequence":"additional","affiliation":[{"name":"University of Queensland Diamantina Institute, Translational Research Institute , Brisbane, Queensland 4102 ,","place":["Australia"]},{"name":"Australian Infectious Diseases Research Centre, University of Queensland , Brisbane, Queensland 4102 ,","place":["Australia"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2014,9,1]]},"reference":[{"key":"2025030707320455800_r1","doi-asserted-by":"crossref","first-page":"607","DOI":"10.1016\/S1470-2045(12)70137-7","article-title":"Global burden of cancers attributable to infections in 2008: a review and synthetic analysis","volume":"13","author":"de Martel","year":"2012","journal-title":"Lancet Oncol."},{"key":"2025030707320455800_r2","doi-asserted-by":"crossref","first-page":"1461","DOI":"10.1016\/S0140-6736(11)61351-2","article-title":"Breast and cervical cancer in 187 countries between 1980 and 2010: a systematic analysis","volume":"378","author":"Forouzanfar","year":"2011","journal-title":"Lancet"},{"key":"2025030707320455800_r3","doi-asserted-by":"crossref","first-page":"890","DOI":"10.1016\/S0140-6736(07)61416-0","article-title":"Human papillomavirus and cervical cancer","volume":"370","author":"Schiffman","year":"2007","journal-title":"Lancet"},{"key":"2025030707320455800_r4","doi-asserted-by":"crossref","first-page":"550","DOI":"10.1038\/nrc2886","article-title":"Human papillomavirus oncoproteins: pathways to transformation","volume":"10","author":"Moody","year":"2010","journal-title":"Nat. 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