PMID- 18243370
OWN - NLM
STAT- MEDLINE
DCOM- 20090922
LR  - 20081222
IS  - 1874-1754 (Electronic)
IS  - 0167-5273 (Linking)
VI  - 131
IP  - 2
DP  - 2009 Jan 9
TI  - Blood dendritic cell levels and phenotypic characteristics in relation to 
      etiology of end-stage heart failure: implications for dilated cardiomyopathy.
PG  - 246-56
LID - 10.1016/j.ijcard.2007.10.031 [doi]
AB  - 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.
FAU - Athanassopoulos, Petros
AU  - Athanassopoulos P
AD  - Department of Cardiothoracic Surgery, Erasmus MC, Rotterdam, The Netherlands. 
      p.athanassopoulos@erasmusmc.nl
FAU - Balk, Aggie H M M
AU  - Balk AH
FAU - Vaessen, Leonard M B
AU  - Vaessen LM
FAU - Caliskan, Kadir
AU  - Caliskan K
FAU - Takkenberg, Johanna J M
AU  - Takkenberg JJ
FAU - Weimar, Willem
AU  - Weimar W
FAU - Bogers, Ad J J C
AU  - Bogers AJ
LA  - eng
PT  - Comparative Study
PT  - Journal Article
DEP - 20080219
PL  - Netherlands
TA  - Int J Cardiol
JT  - International journal of cardiology
JID - 8200291
SB  - IM
MH  - Adult
MH  - Aged
MH  - Cardiomyopathy, Dilated/blood/*immunology/*pathology
MH  - Cross-Sectional Studies
MH  - Dendritic Cells/immunology/*pathology
MH  - Female
MH  - Heart Failure/blood/*immunology/*pathology
MH  - Humans
MH  - *Immunophenotyping
MH  - Male
MH  - Middle Aged
EDAT- 2008/02/05 09:00
MHDA- 2009/09/23 06:00
CRDT- 2008/02/05 09:00
PHST- 2007/04/01 00:00 [received]
PHST- 2007/08/17 00:00 [revised]
PHST- 2007/10/27 00:00 [accepted]
PHST- 2008/02/05 09:00 [pubmed]
PHST- 2009/09/23 06:00 [medline]
PHST- 2008/02/05 09:00 [entrez]
AID - S0167-5273(07)01964-X [pii]
AID - 10.1016/j.ijcard.2007.10.031 [doi]
PST - ppublish
SO  - Int J Cardiol. 2009 Jan 9;131(2):246-56. doi: 10.1016/j.ijcard.2007.10.031. Epub 
      2008 Feb 19.