title: Expression of dendritic cell markers CD11c/BDCA-1 and CD123/BDCA-2 in coronary artery disease upon activation in whole blood.
abstract: OBJECTIVE
  Previous in vivo studies on dendritic cell (DC) enumeration in coronary artery disease (CAD) were not always consistent. Therefore, we investigated by flow cytometry whether this was due to CAD-related differences in expression of subset markers for myeloid (m)DCs (blood DC antigen (BDCA)-1, CD11c) and plasmacytoid (p)DCs (BDCA-2, CD123), before and after in vitro stimulation with Toll-like receptor ligands.
  
  
  RESULTS
  Our data showed that circulating DCs decline in CAD, irrespective of the DC subset marker that was used for enumeration. Upon in vitro activation, BDCA-2 was downregulated, whereas CD11c and CD123 were upregulated. This implies that the expression ratios CD11c/BDCA-1 and CD123/BDCA-2 can assess DC activation. Comparing these ratios between controls and CAD patients showed no differences in blood DC activation in both groups.
  
  
  CONCLUSIONS
  This study suggests that when different DC numbers are found between two study populations, the DC activation status from both groups always needs to be verified, since a decrease in BDCA-2(+) pDCs or an increase in CD11c(+) mDCs or CD123(+) pDCs can be due to the altered expression of these markers during activation. Given that CD11c, BDCA-1, CD123 and BDCA-2 are more abundantly expressed on blood DCs than typical activation markers like CD83, CD86 or CCR-7, the use of the ratios is an easy and reliable way to determine DC activation in whole blood assays.
authors.affiliation: Division of Cardiology, University of Antwerp, Wilrijk, Belgium. ilse.van.brussel@uza.be
authors.forename: Ilse
authors.initials: I
authors.lastname: Van Brussel
authors.forename: Emily A
authors.initials: EA
authors.lastname: Van Vré
authors.forename: Guido R Y
authors.initials: GR
authors.lastname: De Meyer
authors.forename: Christiaan J
authors.initials: CJ
authors.lastname: Vrints
authors.forename: Johan M
authors.initials: JM
authors.lastname: Bosmans
authors.forename: Hidde
authors.initials: H
authors.lastname: Bult
mesh_terms: D018949:Antigens, CD1; D000954:Antigens, Surface / Q000097:blood* / Q000276:immunology; D039521:CD11c Antigen / Q000097:blood* / Q000276:immunology; D003324:Coronary Artery Disease / Q000097:blood* / Q000276:immunology; D003713:Dendritic Cells / Q000276:immunology / Q000378:metabolism*; D005260:Female; D005786:Gene Expression Regulation; D006023:Glycoproteins; D006801:Humans; D053650:Interleukin-3 Receptor alpha Subunit / Q000097:blood* / Q000276:immunology; D037181:Lectins, C-Type / Q000097:blood* / Q000276:immunology; D008297:Male; D008562:Membrane Glycoproteins / Q000097:blood* / Q000276:immunology; D011971:Receptors, Immunologic / Q000097:blood* / Q000276:immunology
chemical_list: D018949:Antigens, CD1; D000954:Antigens, Surface; D039521:CD11c Antigen; C437944:CD1C protein, human; C443299:CLEC4C protein, human; D006023:Glycoproteins; C115022:IL3RA protein, human; D053650:Interleukin-3 Receptor alpha Subunit; D037181:Lectins, C-Type; D008562:Membrane Glycoproteins; D011971:Receptors, Immunologic