{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T08:06:41Z","timestamp":1791274001024,"version":"4.1.0"},"reference-count":36,"publisher":"National Academy of Sciences","issue":"36","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2008,9,9]]},"abstract":"<jats:p>\n                    We report a mechanism of microbial evasion of Toll-like receptor (TLR)-mediated immunity that depends on CXCR4 exploitation. Specifically, the oral\/systemic pathogen\n                    <jats:italic>Porphyromonas gingivalis<\/jats:italic>\n                    induces cross-talk between CXCR4 and TLR2 in human monocytes or mouse macrophages and undermines host defense. This is accomplished through its surface fimbriae, which induce CXCR4\/TLR2 co-association in lipid rafts and interact with both receptors: Binding to CXCR4 induces cAMP-dependent protein kinase A (PKA) signaling, which in turn inhibits TLR2-mediated proinflammatory and antimicrobial responses to the pathogen. This outcome enables\n                    <jats:italic>P. gingivalis<\/jats:italic>\n                    to resist clearance\n                    <jats:italic>in vitro<\/jats:italic>\n                    and\n                    <jats:italic>in vivo<\/jats:italic>\n                    and thus to promote its adaptive fitness. However, a specific CXCR4 antagonist abrogates this immune evasion mechanism and offers a promising counterstrategy for the control of\n                    <jats:italic>P. gingivalis<\/jats:italic>\n                    periodontal or systemic infections.\n                  <\/jats:p>","DOI":"10.1073\/pnas.0803852105","type":"journal-article","created":{"date-parts":[[2008,9,2]],"date-time":"2008-09-02T21:37:12Z","timestamp":1220391432000},"page":"13532-13537","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":176,"title":["Pathogen induction of CXCR4\/TLR2 cross-talk impairs host defense function"],"prefix":"10.1073","volume":"105","author":[{"given":"George","family":"Hajishengallis","sequence":"first","affiliation":[{"name":"*Division of Oral Health and Systemic Disease\/Department of Periodontics and"},{"name":"Department of Microbiology and Immunology, University of Louisville Health Sciences Center, Louisville, KY 40292; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Min","family":"Wang","sequence":"additional","affiliation":[{"name":"*Division of Oral Health and Systemic Disease\/Department of Periodontics and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shuang","family":"Liang","sequence":"additional","affiliation":[{"name":"*Division of Oral Health and Systemic Disease\/Department of Periodontics and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martha","family":"Triantafilou","sequence":"additional","affiliation":[{"name":"Infection and Immunity Group, School of Life Sciences, University of Sussex, Falmer, Brighton BN1 9QG, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kathy","family":"Triantafilou","sequence":"additional","affiliation":[{"name":"Infection and Immunity Group, School of Life Sciences, University of Sussex, Falmer, Brighton BN1 9QG, United 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