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Title
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Changes in blood dendritic cell counts in relation to type of coronary artery disease and brachial endothelial cell function
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Author
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Abstract
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| Background Recently we reported a decline of circulating myeloid (m) and plasmacytoid (p) dendritic cells (DCs) in patients with coronary artery disease (CAD). This study also determined the total blood DC numbers and focused on effects of extent (one vs. three-vessel disease) and type (stable vs. unstable) of CAD, and on endothelial cell function. Methods Patients undergoing diagnostic coronarography were enrolled in four groups: control patients (atypical chest pain, <50% narrowing, n=15), stable one-vessel (n=15), stable three-vessel (n=15), and unstable one-vessel CAD (n=16). Total blood DCs were identified as lineage (lin) and HLADR+ , and DC subtypes with blood DC antigen (BDCA)-1+ formDCs and BDCA-2+ for pDCs. Flow-mediated dilatation (FMD) was measured in the brachial artery. Results Numbers of total blood DCs, mDCs and pDCs declined in CAD patients compared with control patients, but without differences between the CAD groups. Interleukin-6 and high sensitivity C-reactive protein displayed inverse associations with mDCs. A FMD below the median of the study population, use of b-blockers or of lipid-lowering drugs was associated with increased mDCs, whereas pDCs were similar. Interestingly, the effects of drugs and FMD were additive with that of CAD. Conclusion This study indicates that lower blood DCs do not result from medication intake or endothelial dysfunction, and are an overall systemic effect of atherosclerosis rather than CAD type (stable or unstable) or number of stenotic coronary arteries. In view of discrete associations with cytokines, FMD, b-blockers and statins, mDCs and pDCs seem to behave differently and may influence inflammation during atherosclerosis in different ways. |
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Language
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English
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Source (journal)
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Coronary artery disease. - Philadelphia, Pa
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Publication
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Philadelphia, Pa
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2010
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ISSN
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0954-6928
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DOI
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10.1097/MCA.0B013E3283368C0E
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Volume/pages
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21
:2
(2010)
, p. 87-96
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ISI
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000279667700005
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Full text (Publisher's DOI)
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Full text (publisher's version - intranet only)
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