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Reduction and activation of circulating dendritic cells in patients with decompensated heart failure.

Abstract：

BACKGROUND:Dendritic cells (DCs) are the most potent antigen-presenting cells and play a central role in initiating the primary immune response. Although increasing evidence supports immune-mediated inflammation plays an important role in the pathophysiology of heart failure, little is known regarding the source and mechanism that trigger immune responses. The present study examined whether circulating DCs have any role in the pathophysiology in heart failure in humans. METHODS AND RESULTS:With multi-color flow cytometry we determined the numbers of circulating myeloid DCs (mDCs) and plasmacytoid DCs (pDCs) in decompensated heart failure patients with NYHA class III or IV on admission (n = 27) and the age-similar control subjects (n = 21). DC activation markers such as CD40, and CCR7 were also measured. On admission, circulating mDC and pDC counts were significantly lower in decompensated heart failure patients compared to control subjects (p < 0.01). Circulating mDCs and pDCs were activated in the decompensated heart failure patients. Heart failure treatment restored the reduction and the activation of circulating mDCs and pDCs (p < 0.05). The increases of circulating DCs numbers after treatment were correlated with the decreases in B-type natriuretic peptide (BNP) and troponin-T (p < 0.05) and with the increase in left ventricular ejection fraction (LVEF) (p < 0.01). Furthermore, we found that poor recovery of the circulating DCs number after treatment predicted recurrence of decompensated heart failure. CONCLUSION:These findings suggest that the reduction and activation of circulating DCs may be involved in the pathophysiology of heart failure.

journal_name

Int J Cardiol

journal_title

International journal of cardiology

authors

Sugi Y,Yasukawa H,Kai H,Fukui D,Futamata N,Mawatari K,Oba T,Nagata N,Kyougoku S,Koga M,Imaizumi T

doi

10.1016/j.ijcard.2009.09.524

subject

Has Abstract

pub_date

2011-03-03 00:00:00

pages

258-64

issue

2

eissn

0167-5273

issn

1874-1754

pii

S0167-5273(09)01466-1

journal_volume

147

pub_type

杂志文章

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