{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T10:50:36Z","timestamp":1789728636808,"version":"4.0.1"},"reference-count":59,"publisher":"Oxford University Press (OUP)","issue":"11","license":[{"start":{"date-parts":[[2009,12,1]],"date-time":"2009-12-01T00:00:00Z","timestamp":1259625600000},"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":[[2009,12,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Chronic systemic inflammation links periodontal disease and diabetes to increased incidence of serious comorbidities. Activation of TLRs, particularly TLR2 and TLR4, promotes chronic systemic inflammation. Human B cells have been generally thought to lack these TLRs. However, recent work showed that an increased percentage of circulating B cells from inflammatory disease patients express TLR2 and TLR4, and that TLR engagement on B cells resulted in unexpected changes in gene expression. New data show that B cells from inflammatory disease patients secrete multiple cytokines in response to different classes of TLR ligands. Furthermore, the B cell response to combinations of TLR ligands is cytokine- and ligand-specific. Some cytokines (IL-1\u03b2 and IL-10) are predominantly regulated by TLR4, but others (IL-8 and TNF-\u03b1) are predominantly regulated by TLR2, due in part to TLR-dictated changes in transcription factor\/promoter association. TLR2 and TLR9 also regulate B cell TLR4 expression, demonstrating that TLR cross-talk controls B cell responses at multiple levels. Parallel examination of B cells from periodontal disease and diabetes patients suggested that outcomes of TLR cross-talk are influenced by disease pathology. We conclude that disease-associated alteration of B cell TLR responses specifically regulates cytokine production and may influence chronic inflammation.<\/jats:p>","DOI":"10.4049\/jimmunol.0901517","type":"journal-article","created":{"date-parts":[[2009,11,16]],"date-time":"2009-11-16T21:55:14Z","timestamp":1258408514000},"page":"7461-7470","source":"Crossref","is-referenced-by-count":82,"title":["TLR Cross-Talk Specifically Regulates Cytokine Production by B Cells from Chronic Inflammatory Disease Patients"],"prefix":"10.1093","volume":"183","author":[{"given":"Madhumita","family":"Jagannathan","sequence":"first","affiliation":[{"name":"Department of Pathology, Boston University School of Medicine , Boston, MA 02118"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hatice","family":"Hasturk","sequence":"additional","affiliation":[{"name":"Department of Periodontology and Oral Biology, Boston University Goldman School of Dental Medicine , Boston, MA 02118"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"YanMei","family":"Liang","sequence":"additional","affiliation":[{"name":"Department of Medicine, Section of Infectious Diseases, Evans Biomedical Research Center, Boston Medical Center , Boston, MA 02118"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hyunjin","family":"Shin","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Boston University School of Medicine , Boston, MA 02118"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeremy T","family":"Hetzel","sequence":"additional","affiliation":[{"name":"Department of Medicine, Section of Endocrinology, Boston Medical Center , Boston, MA 02118"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alpdogan","family":"Kantarci","sequence":"additional","affiliation":[{"name":"Department of Periodontology and Oral Biology, Boston University Goldman School of Dental Medicine , Boston, MA 02118"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel","family":"Rubin","sequence":"additional","affiliation":[{"name":"Department of Medicine, Section of Endocrinology, Boston Medical Center , Boston, MA 02118"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marie E","family":"McDonnell","sequence":"additional","affiliation":[{"name":"Department of Medicine, Section of Endocrinology, Boston Medical Center , Boston, MA 02118"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas E","family":"Van Dyke","sequence":"additional","affiliation":[{"name":"Department of Periodontology and Oral Biology, Boston University Goldman School of Dental Medicine , Boston, MA 02118"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lisa M","family":"Ganley-Leal","sequence":"additional","affiliation":[{"name":"Department of Medicine, Section of Infectious Diseases, Evans Biomedical Research Center, Boston Medical Center , Boston, MA 02118"},{"name":"Department of Microbiology, Boston University School of Medicine , Boston, MA 02118"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Barbara S","family":"Nikolajczyk","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Boston University School of Medicine , Boston, MA 02118"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2009,12,1]]},"reference":[{"key":"2026012811272505600_R1","first-page":"59","article-title":"Cardiovascular and oral disease interactions: what is the evidence?.","volume-title":"Prim. 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