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Blood dendritic cell levels and phenotypic characteristics in relation to etiology of end-stage heart failure: implications for dilated cardiomyopathy.

Abstract：

BACKGROUND:Dysregulation of dendritic cell (DC) mediated immune responses towards auto-antigens, is considered an important feature in the maintenance of experimentally induced heart failure (HF). In order to evaluate the role of blood DCs in cardiomyopathies of different origins, we examined myeloid (mDC) and plasmacytoid (pDC) subset levels and maturation characteristics, according to HF severity and etiology in humans. METHODS:Absolute numbers of mDCs and pDCs in 12 New York Heart Association (NYHA) class-II, 28 NYHA class III-IV HF patients and 18 healthy controls, were studied by 4-colour whole blood flow cytometry. RESULTS:End-stage (NYHA III-IV) HF patients had comparable circulating DC subset levels to NYHA-II patients and controls. However, within the NYHA III-IV group total DC levels in patients with non-ischemic dilated cardiomyopathy (DCM) were higher (P<0.001) than in patients with coronary artery disease (CAD), hypertrophic cardiomyopathy (HCM) or other HF etiology. This was due to a significant increase of primarily mDCs (P<0.0001) and to a lesser extent of pDCs (P<0.05) in idiopathic DCM patients, independent of systolic or diastolic cardiac dysfunction. Maturation marker CD83 and lymphoid homing chemokine receptor CCR7 surface expression was enhanced only on mDCs, but not pDCs from DCM patients (P<0.05), compared to patients with CAD, HCM or other underlying cardiac pathophysiology. CONCLUSIONS:Total blood DC levels in end-stage HF are elevated in patients with DCM. Whole blood DC characterisation may lead to new insights into the pathophysiology of idiopathic DCM in humans.

journal_name

Int J Cardiol

journal_title

International journal of cardiology

authors

Athanassopoulos P,Balk AH,Vaessen LM,Caliskan K,Takkenberg JJ,Weimar W,Bogers AJ

doi

10.1016/j.ijcard.2007.10.031

subject

Has Abstract

pub_date

2009-01-09 00:00:00

pages

246-56

issue

2

eissn

0167-5273

issn

1874-1754

pii

S0167-5273(07)01964-X

journal_volume

131

pub_type

杂志文章

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