Letter to the Editor doi:10.1093/eurheartj/ehi633

The role of dendritic cells in specific atherosclerosis types: reply In the article entitled ‘Dendritic cells in atherosclerosis: current status of the problem and clinical relevance’, I have reviewed the current knowledge relating to the role of dendritic cells (DCs) in athero-sclerosis. The studies of the involvement of DCs in other vascular diseases, such as aortic aneurysm1 and vasculitis,2,3 as well as the studies of DCs in venous pathologies have not been highlighted in the review. The acknowledgement of the studies of DCs in aortocoronary saphenous vein bypass grafts, vascular synthetic grafts,4 in-stent restenosis (ISR),5 and in arteries after balloon injury 6 has been beyond the scope of the review. Over the last decades, the properties of DCs were intensely studied and much know-ledge has been gained about the role of DCs in various diseases and health conditions where the immune system is involved. In contrast, studies investigating a possible contribution of DCs in health conditions where the immune system is not involved or is minimally involved are scanty. In this respect, the works of Bauriedel and co-workers5,6 are of special interest and import-ance. Bauriedel et al.6 have shown that, in early stages of neointima formation, DCs may provide coordinated anti-apoptotic signals that are essential for the mainten-ance of cellular integrity of the arterial wall, while neointimal tissue consolidation occurs. Bauriedel and co-workers5 have also identified DCs in human ISR atherectomy tissue samples, and it has been shown that the frequency of DCs in tissue samples obtained from patients with clinical ISR was markedly higher than those in tissue samples representing de novo lesions.5 The study of DCs in vascular pathologies is in its infancy. Experimental studies have shown that there is a link between arterial immune inflammation and hypercholestero-laemia, mediated by DCs, and that dislipi-daemia associated with atherosclerotic disease systemically alters the DC function. As highlighted in the review, the accumu-lated evidence indicates that DCs might be importantly involved in plaque destabiliza-tion. I agree with Bauriedel and co-workers that the impact of DCs on plaque destabiliza-tion requires clarification