Decrease in dendritic cells in endomyocardial biopsies of human dilated cardiomyopathy

作者:Pistulli Rudin*; Koenig Sebastian; Drobnik Stefanie; Kretzschmar Daniel; Rohm Ilonka; Lichtenauer Michael; Fritzenwanger Michael; Mall Gerhard; Mall Gita; Figulla Hans Reiner; Yilmaz Atilla
来源:European Journal of Heart Failure, 2013, 15(9): 974-985.
DOI:10.1093/eurjhf/hft054

摘要

Dendritic cells (DCs) are sentinels of the immune systemutheir role in myocardial disease is unknown as yet. We investigated their myocardial presence in human dilated cardiomyopathy (DCM). %26lt;br%26gt;Endomyocardial biopsies from 72 patients with DCM (EF 30), as well as myocardial specimens from 18 suicide or accident victims were immunohistochemically analysed for myeloid and plasmacytoid DCs, antigen-presenting cells (APCs), and other leucocytes; also tissue fibrosis and apoptosis were histologically quantified. The myocardial viral genome was identified through polymerase chain reaction, and patients underwent clinical follow-up in 36 months. We found myocardial DCs of all examined subtypes and maturation stages (fascin, CD11c, CD209, CD83, and CD304), as well as markers for APCs (HLA-DR and CD40) and T-cell activation (CD69) to be significantly decreased in DCM compared with controls. In contrast, regulatory T cells (the GITR epitope), apoptosis (by TUNEL reaction and immunostaining with BCL-2), and a DC chemokine receptor (CCR7) were overexpressed, while no significant differences were observed for macrophages (CD68). Immature myeloid and plasmacytoid DCs strongly correlated with endothelial progenitor cells (CD34), which were similarly reduced in DCM, and inversely correlated with fibrosis. Myeloid DCs were especially reduced in virus-positive biopsies, and their numbers correlated with positive change in EF (EF) at follow-up. %26lt;br%26gt;Myocardial DCs are reduced in heart biopsies of symptomatic DCM patients. Such a reduction correlates with an unfavourable short-term outcome in terms of EF, and could result from myocardial tissue damage, cellular death, and insufficient vascularization in chronic heart failure.

  • 出版日期2013-9