PMID- 24551105
OWN - NLM
STAT- MEDLINE
DCOM- 20141021
LR  - 20211021
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 9
IP  - 2
DP  - 2014
TI  - Dendritic cell subset distributions in the aorta in healthy and atherosclerotic 
      mice.
PG  - e88452
LID - 10.1371/journal.pone.0088452 [doi]
LID - e88452
AB  - Dendritic cells (DCs) can be sub-divided into various subsets that play 
      specialized roles in priming of adaptive immune responses. Atherosclerosis is 
      regarded as a chronic inflammatory disease of the vessel wall and DCs can be 
      found in non-inflamed and diseased arteries. We here performed a systematic 
      analyses of DCs subsets during atherogenesis. Our data indicate that distinct DC 
      subsets can be localized in the vessel wall. In C57BL/6 and low density 
      lipoprotein receptor-deficient (Ldlr (-/-)) mice, CD11c(+) MHCII(+) DCs could be 
      discriminated into CD103(-) CD11b(+)F4/80(+), CD11b(+)F4/80(-) and 
      CD11b(-)F4/80(-) DCs and CD103(+) CD11b(-)F4/80(-) DCs. Except for CD103(-) 
      CD11b(-) F4/80(-) DCs, these subsets expanded in high fat diet-fed Ldlr (-/-) 
      mice. Signal-regulatory protein (Sirp)-alpha was detected on aortic macrophages, 
      CD11b(+) DCs, and partially on CD103(-) CD11b(-) F4/80(-) but not on CD103(+) 
      DCs. Notably, in FMS-like tyrosine kinase 3-ligand-deficient (Flt3l (-/-)) mice, 
      a specific loss of CD103(+) DCs but also CD103(-) CD11b(+) F4/80(-) DCs was 
      evidenced. Aortic CD103(+) and CD11b(+) F4/80(-) CD103(-) DCs may thus belong to 
      conventional rather than monocyte-derived DCs, given their dependence on 
      Flt3L-signalling. CD64, postulated to distinguish macrophages from DCs, could not 
      be detected on DC subsets under physiological conditions, but appeared in a 
      fraction of CD103(-) CD11b(+) F4/80(-) and CD11b(+) F4/80(+) cells in 
      atherosclerotic Ldlr (-/-) mice. The emergence of CD64 expression in 
      atherosclerosis may indicate that CD11b(+) F4/80(-) DCs similar to CD11b(+) 
      F4/80(+) DCs are at least in part derived from immigrated monocytes during 
      atherosclerotic lesion formation. Our data advance our knowledge about the 
      presence of distinct DC subsets and their accumulation characteristics in 
      atherosclerosis, and may help to assist in future studies aiming at specific 
      DC-based therapeutic strategies for the treatment of chronic vascular 
      inflammation.
FAU - Busch, Martin
AU  - Busch M
AD  - Rudolf Virchow-Center; University of Wurzburg, Wurzburg, Germany.
FAU - Westhofen, Thilo C
AU  - Westhofen TC
AD  - Rudolf Virchow-Center; University of Wurzburg, Wurzburg, Germany.
FAU - Koch, Miriam
AU  - Koch M
AD  - Rudolf Virchow-Center; University of Wurzburg, Wurzburg, Germany ; Institute of 
      Clinical Biochemistry and Pathobiocchemistry, University Hospital Wurzburg, 
      Wurzburg, Germany.
FAU - Lutz, Manfred B
AU  - Lutz MB
AD  - Institute of Virology and Immunobiology, University of Wurzburg, Wurzburg, 
      Germany.
FAU - Zernecke, Alma
AU  - Zernecke A
AD  - Institute of Clinical Biochemistry and Pathobiocchemistry, University Hospital 
      Wurzburg, Wurzburg, Germany ; Department of Vascular Surgery, Klinikum rechts der 
      Isar der Technischen Universitat Munchen, Munich, Germany.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140214
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (CD11c Antigen)
RN  - 0 (Ptpns1 protein, mouse)
RN  - 0 (Receptors, IgG)
RN  - 0 (Receptors, Immunologic)
SB  - IM
MH  - Animals
MH  - Aorta/*immunology/*pathology
MH  - Atherosclerosis/*immunology/*pathology
MH  - CD11c Antigen/metabolism
MH  - Dendritic Cells/*immunology
MH  - Macrophages/metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Receptors, IgG/metabolism
MH  - Receptors, Immunologic/metabolism
PMC - PMC3925240
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2014/02/20 06:00
MHDA- 2014/10/22 06:00
PMCR- 2014/02/14
CRDT- 2014/02/20 06:00
PHST- 2013/03/26 00:00 [received]
PHST- 2014/01/10 00:00 [accepted]
PHST- 2014/02/20 06:00 [entrez]
PHST- 2014/02/20 06:00 [pubmed]
PHST- 2014/10/22 06:00 [medline]
PHST- 2014/02/14 00:00 [pmc-release]
AID - PONE-D-13-12426 [pii]
AID - 10.1371/journal.pone.0088452 [doi]
PST - epublish
SO  - PLoS One. 2014 Feb 14;9(2):e88452. doi: 10.1371/journal.pone.0088452. eCollection 
      2014.