| Autor: |
Jagannathan M; Department of Pathology, Boston University School of Medicine, Boston, MA 02118, USA., Hasturk H, Liang Y, Shin H, Hetzel JT, Kantarci A, Rubin D, McDonnell ME, Van Dyke TE, Ganley-Leal LM, Nikolajczyk BS |
| Jazyk: |
angličtina |
| Zdroj: |
Journal of immunology (Baltimore, Md. : 1950) [J Immunol] 2009 Dec 01; Vol. 183 (11), pp. 7461-70. Date of Electronic Publication: 2009 Nov 16. |
| DOI: |
10.4049/jimmunol.0901517 |
| Abstrakt: |
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-1beta and IL-10) are predominantly regulated by TLR4, but others (IL-8 and TNF-alpha) 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. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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