{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,15]],"date-time":"2026-01-15T13:38:26Z","timestamp":1768484306799,"version":"3.49.0"},"reference-count":43,"publisher":"American Society for Microbiology","issue":"7","license":[{"start":{"date-parts":[[2016,7,1]],"date-time":"2016-07-01T00:00:00Z","timestamp":1467331200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/100000060","name":"HHS | NIH | National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["AI29735"],"award-info":[{"award-number":["AI29735"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000060","name":"HHS | NIH | National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["AI085248"],"award-info":[{"award-number":["AI085248"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000072","name":"HHS | NIH | National Institute of Dental and Craniofacial Research","doi-asserted-by":"publisher","award":["DE017401"],"award-info":[{"award-number":["DE017401"]}],"id":[{"id":"10.13039\/100000072","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000072","name":"HHS | NIH | National Institute of Dental and Craniofacial Research","doi-asserted-by":"publisher","award":["DE023000"],"award-info":[{"award-number":["DE023000"]}],"id":[{"id":"10.13039\/100000072","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000072","name":"HHS | NIH | National Institute of Dental and Craniofacial Research","doi-asserted-by":"publisher","award":["DE0233080"],"award-info":[{"award-number":["DE0233080"]}],"id":[{"id":"10.13039\/100000072","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2016,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            The\n            <jats:named-content content-type=\"genus-species\">Treponema denticola<\/jats:named-content>\n            FhbB protein contributes to immune evasion by binding factor H (FH). Cleavage of FH by the\n            <jats:named-content content-type=\"genus-species\">T. denticola<\/jats:named-content>\n            protease, dentilisin, may contribute to the local immune dysregulation that is characteristic of periodontal disease (PD). Although three FhbB phyletic types have been defined (FhbB1, FhbB2, and FhbB3), the\n            <jats:italic>in vivo<\/jats:italic>\n            expression patterns and antigenic heterogeneity of FhbB have not been assessed. Here, we demonstrate that FhbB is a dominant early antigen that elicits FhbB type-specific antibody (Ab) responses. Using the murine skin abscess model, we demonstrate that the presence or absence of FhbB or dentilisin significantly influences Ab responses to infection and skin abscess formation. Competitive binding analyses revealed that \u03b1-FhbB Ab can compete with FH for binding to\n            <jats:named-content content-type=\"genus-species\">T. denticola<\/jats:named-content>\n            and block dentilisin-mediated FH cleavage. Lastly, we demonstrate that dentilisin cleavage sites reside within critical functional domains of FH, including the complement regulatory domain formed by CCPs 1 to 4. Analysis of the FH cleavage products revealed that they lack cofactor activity. The data presented here provide insight into the\n            <jats:italic>in vivo<\/jats:italic>\n            significance of dentilisin, FhbB and its antigenic diversity, and the potential impact of FH cleavage on the regulation of complement activation.\n          <\/jats:p>","DOI":"10.1128\/iai.01542-15","type":"journal-article","created":{"date-parts":[[2016,4,26]],"date-time":"2016-04-26T03:49:42Z","timestamp":1461642582000},"page":"2051-2058","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":22,"title":["The Treponema denticola FhbB Protein Is a Dominant Early Antigen That Elicits FhbB Variant-Specific Antibodies That Block Factor H Binding and Cleavage by Dentilisin"],"prefix":"10.1128","volume":"84","author":[{"given":"Daniel P.","family":"Miller","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, Virginia Commonwealth University Medical Center, Richmond, Virginia, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"suffix":"Jr.","given":"Lee D.","family":"Oliver","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Virginia Commonwealth University Medical Center, Richmond, Virginia, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Brittney K.","family":"Tegels","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Virginia Commonwealth University Medical Center, Richmond, Virginia, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lucas A.","family":"Reed","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Virginia Commonwealth University Medical Center, Richmond, Virginia, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nathaniel S.","family":"O'Bier","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Virginia Commonwealth 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