{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T07:41:55Z","timestamp":1792568515419,"version":"4.5.0"},"reference-count":35,"publisher":"Wiley","license":[{"start":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T00:00:00Z","timestamp":1792540800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T00:00:00Z","timestamp":1792540800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100003725","name":"National Research Foundation of Korea","doi-asserted-by":"publisher","award":["#RS\u20102024\u201000342340"],"award-info":[{"award-number":["#RS\u20102024\u201000342340"]}],"id":[{"id":"10.13039\/501100003725","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Molecular Oral Microbiology"],"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    While Th1 and Th17 cells are well known for their distinct roles in host defense, how these effector CD4\n                    <jats:sup>+<\/jats:sup>\n                    T\u2010cell subsets influence epithelial responses to intracellular bacteria remains unclear. Here, we investigated whether Th1 or Th17 cells modulate the intracellular survival of\n                    <jats:italic>Escherichia coli<\/jats:italic>\n                    7.2 (Ec7.2), a clinical isolate from oral lichen planus (OLP) tissue, in oral keratinocytes. To assess antigen\u2010specific and antigen\u2010independent T\u2010cell effects, we established a co\u2010culture system using IFN\u2010\u03b3\u2010pretreated, Ec7.2\u2010infected immortalized murine oral keratinocytes (IMOK) and Th1 or Th17 cells differentiated from OT\u2010II\u2010restricted CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells, in the absence or presence of cognate peptide. Th1 cells reduced intracellular Ec7.2 in an antigen\u2010dependent manner, whereas Th17 cells consistently increased bacterial persistence through largely antigen\u2010independent and contact\u2010independent mechanisms. Transcriptomic analysis of infected IMOK cells revealed that Th17\u2010associated soluble signals broadly attenuated epithelial innate immune and antibacterial responses, including pathways related to type II interferon signaling, chemokine production, and defense response to bacterium. Among these,\n                    <jats:italic>Nos2<\/jats:italic>\n                    expression was significantly reduced upon Th17 co\u2010culture and was accompanied by decreased nitric oxide (NO) production. Th17 cells expressed higher levels of\n                    <jats:italic>Tgfb1<\/jats:italic>\n                    than Th1 cells, and elevated TGF\u2010\u03b2 concentrations were consistently observed under Th17 co\u2010culture conditions associated with increased bacterial persistence. Neutralization of TGF\u2010\u03b2 was associated with a trend toward increased NO production and reduced intracellular Ec7.2 recovery relative to isotype\u2010treated controls. Together, these findings identify a previously underappreciated role for Th17\u2013associated signals in modulating epithelial defense against intracellular bacteria, in part through TGF\u2010\u03b2\u2013associated suppression of NO\u2010associated antimicrobial responses, which may contribute to bacterial persistence in Th17\u2010dominated mucosal environments.\n                  <\/jats:p>","DOI":"10.1111\/omi.70043","type":"journal-article","created":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T07:10:11Z","timestamp":1792566611000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Th17 Cells Impair Epithelial Defense Against Intracellular Bacteria in Part Through TGF\u2010\u03b2"],"prefix":"10.1111","author":[{"given":"Mingyu","family":"Kang","sequence":"first","affiliation":[{"name":"Department of Immunology and Molecular Microbiology in Dental Science, School of Dentistry and Dental Research Institute Seoul National University  Seoul Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hyeong\u2010jin","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Immunology and Molecular Microbiology in Dental Science, School of Dentistry and Dental Research Institute Seoul National University  Seoul Republic of Korea"},{"name":"Chayon Laboratories, Inc.  Seoul Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jieun","family":"Song","sequence":"additional","affiliation":[{"name":"Department of Immunology and Molecular Microbiology in Dental Science, School of Dentistry and Dental Research Institute Seoul National University  Seoul Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0008-9953-4817","authenticated-orcid":false,"given":"Sabin","family":"Acharya","sequence":"additional","affiliation":[{"name":"Department of Immunology and Molecular Microbiology in Dental Science, School of Dentistry and Dental Research Institute Seoul National University  Seoul Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6496-5560","authenticated-orcid":false,"given":"Youngnim","family":"Choi","sequence":"additional","affiliation":[{"name":"Department of Immunology and Molecular Microbiology in 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