{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T03:59:10Z","timestamp":1790395150737,"version":"4.1.0"},"reference-count":43,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2016,8,1]],"date-time":"2016-08-01T00:00:00Z","timestamp":1470009600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100000268","name":"Biotechnology and Biological Sciences Research Council","doi-asserted-by":"publisher","award":["BB\/M503289\/1"],"award-info":[{"award-number":["BB\/M503289\/1"]}],"id":[{"id":"10.13039\/501100000268","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000341","name":"Arthritis Research UK","doi-asserted-by":"publisher","award":["19307"],"award-info":[{"award-number":["19307"]}],"id":[{"id":"10.13039\/501100000341","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[2016,9]]},"abstract":"\n The Th17\/IL\u201017 pathway is implicated in the pathogenesis of periodontitis (PD), however the mechanisms are not fully understood. We investigated the mechanism by which the periodontal pathogens\n Porphyromonas gingivalis<\/jats:italic>\n (\n Pg<\/jats:italic>\n ) and\n Aggregatibacter actinomycetemcomitans<\/jats:italic>\n (\n Aa<\/jats:italic>\n ) promote a Th17\/IL\u201017 response in vitro, and studied IL\u201017\n +<\/jats:sup>\n CD4\n +<\/jats:sup>\n T\u2010cell frequencies in gingival tissue and peripheral blood from patients with PD versus periodontally healthy controls. Addition of\n Pg<\/jats:italic>\n or\n Aa<\/jats:italic>\n to monocyte\/CD4\n +<\/jats:sup>\n T\u2010cell co\u2010cultures promoted a Th17\/IL\u201017 response in vitro in a dose\u2010 and time\u2010dependent manner.\n Pg<\/jats:italic>\n or\n Aa<\/jats:italic>\n stimulation of monocytes resulted in increased CD40, CD54 and HLA\u2010DR expression, and enhanced TNF\u2010\u03b1, IL\u20101\u03b2, IL\u20106 and IL\u201023 production. Mechanistically, IL\u201017 production in\n Pg<\/jats:italic>\n \u2010stimulated co\u2010cultures was partially dependent on IL\u20101\u03b2, IL\u201023 and TLR2\/TLR4 signalling. Increased frequencies of IL\u201017\n +<\/jats:sup>\n cells were observed in gingival tissue from patients with PD compared to healthy subjects. No differences were observed in IL\u201017\n +<\/jats:sup>\n CD4\n +<\/jats:sup>\n T\u2010cell frequencies in peripheral blood. In vitro,\n Pg<\/jats:italic>\n induced significantly higher IL\u201017 production in anti\u2010CD3 mAb\u2010stimulated monocyte\/CD4\n +<\/jats:sup>\n T\u2010cell co\u2010cultures from patients with PD compared to healthy controls. Our data suggest that periodontal pathogens can activate monocytes, resulting in increased IL\u201017 production by human CD4\n +<\/jats:sup>\n T cells, a process that appears enhanced in patients with PD.\n <\/jats:p>","DOI":"10.1002\/eji.201545871","type":"journal-article","created":{"date-parts":[[2016,6,23]],"date-time":"2016-06-23T05:33:39Z","timestamp":1466660019000},"page":"2211-2221","source":"Crossref","is-referenced-by-count":81,"title":["Periodontitis\u2010associated pathogens\n P. gingivalis<\/i>\n and\n A. actinomycetemcomitans<\/i>\n activate human CD14\n +<\/sup>\n monocytes leading to enhanced Th17\/IL\u201017 responses"],"prefix":"10.1002","volume":"46","author":[{"given":"Wan\u2010Chien","family":"Cheng","sequence":"first","affiliation":[{"name":"Division of Immunology Infection & Inflammatory Disease Centre for Molecular and Cellular Biology of Inflammation King's College London London UK"},{"name":"Department of Periodontology Dental Institute King's College London London UK"},{"name":"Department of Periodontology School of Dentistry Tri\u2010Service General Hospital and National Defense Medical Center Taipei Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Saskia D.","family":"van Asten","sequence":"additional","affiliation":[{"name":"Division of Immunology Infection & Inflammatory Disease Centre for Molecular and Cellular Biology of Inflammation King's College London London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lachrissa A.","family":"Burns","sequence":"additional","affiliation":[{"name":"Division of Immunology Infection & Inflammatory Disease Centre for Molecular and Cellular Biology of Inflammation King's College London London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hayley G.","family":"Evans","sequence":"additional","affiliation":[{"name":"Division of Immunology Infection & Inflammatory Disease Centre for Molecular and Cellular Biology of Inflammation King's 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