title: Immunohistochemical characterisation of dendritic cells in human atherosclerotic lesions: possible pitfalls.
abstract: BACKGROUND
  Previously we demonstrated decreased blood myeloid (m) and plasmacytoid (p) dendritic cell (DC) counts in atherosclerotic patients. Therefore, we examined whether DCs, in particular DC precursors, accumulate in human plaques.
  
  
  METHODS
  Blood DC antigen (BDCA)-1, CD11c (mDCs), BDCA-2, CD123 (pDCs), langerin, fascin, S-100 (immature/mature DCs), and CD1a and CD83 (mature DCs) were investigated by immunohistochemistry of carotid arteries obtained by endarterectomy (EAS, frozen n = 11, fixed n = 11) or autopsy (fixed, n = 87).
  
  
  RESULTS
  Fascin and S-100 required formaldehyde fixation, other markers needed cryo-preservation. BDCA-1, BDCA-2, langerin, and S-100 appeared specific for intimal DCs, unlike CD123 and fascin (staining endothelial cells), CD11c and CD1a (staining monocytes, foam cells) or CD83 (staining lymphocytes). BDCA-1 and BDCA-2 cells were detected in EAS, preferentially near microvessels. S-100 cells increased successively from intimal thickening, via pathological intimal thickening, fibrous cap atheroma and finally complicated plaques. Fascin cells followed the same pattern, but were more abundant. However, in lesions containing microvessels (complicated plaques, plaque shoulders and most EAS) this was partly explained by fascin positive endothelial cells. Even complicated plaques contained relatively few mature CD83 DCs.
  
  
  CONCLUSIONS
  Accumulation of BDCA-1 and BDCA-2 around neovessels showed that mDCs and pDCs are recruited to advanced plaques, which is in line with the previously described decline of circulating blood DCs in patients with coronary artery disease. Unexpectedly, several DC markers yielded false positive signals. Hence, some accounts on numbers, trafficking and activation of DCs in atherosclerotic plaques may require re-evaluation.
authors: Division of Cardiology, Department of Translational Pathophysiological Research, University of Antwerp, Wilrijk, Belgium.
authors: Emily A
authors: EA
authors: Van Vré
authors: Johan M
authors: JM
authors: Bosmans
authors: Ilse
authors: I
authors: Van Brussel
authors: Mieke
authors: M
authors: Maris
authors: Guido R Y
authors: GR
authors: De Meyer
authors: Paul E
authors: PE
authors: Van Schil
authors: Christiaan J
authors: CJ
authors: Vrints
authors: Hidde
authors: H
authors: Bult
mesh_terms: D018949:Antigens, CD1; D000954:Antigens, Surface / Q000378:metabolism; D050197:Atherosclerosis / Q000378:metabolism / Q000473:pathology*; D015415:Biomarkers / Q000378:metabolism; D002339:Carotid Arteries / Q000378:metabolism / Q000473:pathology / Q000601:surgery; D003713:Dendritic Cells / Q000378:metabolism / Q000473:pathology*; D016894:Endarterectomy, Carotid; D019084:Fluorescent Antibody Technique, Indirect; D006023:Glycoproteins; D006801:Humans; D037181:Lectins, C-Type / Q000378:metabolism; D008562:Membrane Glycoproteins / Q000378:metabolism; D058226:Plaque, Atherosclerotic / Q000378:metabolism / Q000473:pathology*; D011971:Receptors, Immunologic / Q000378:metabolism
chemical_list: D018949:Antigens, CD1; D000954:Antigens, Surface; D015415:Biomarkers; C437944:CD1C protein, human; C443299:CLEC4C protein, human; D006023:Glycoproteins; D037181:Lectins, C-Type; D008562:Membrane Glycoproteins; D011971:Receptors, Immunologic