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 for mDCs 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 
beta-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, beta-blockers and statins, mDCs and pDCs seem to behave differently and may 
influence inflammation during atherosclerosis in different ways.