PMID- 28771609
OWN - NLM
STAT- MEDLINE
DCOM- 20171006
LR  - 20181113
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 12
IP  - 8
DP  - 2017
TI  - Deletion of Batf3-dependent antigen-presenting cells does not affect 
      atherosclerotic lesion formation in mice.
PG  - e0181947
LID - 10.1371/journal.pone.0181947 [doi]
LID - e0181947
AB  - Atherosclerosis is the main underlying cause for cardiovascular events such as 
      myocardial infarction and stroke and its development might be influenced by 
      immune cells. Dendritic cells (DCs) bridge innate and adaptive immune responses 
      by presenting antigens to T cells and releasing a variety of cytokines. Several 
      subsets of DCs can be discriminated that engage specific transcriptional pathways 
      for their development. Basic leucine zipper transcription factor ATF-like 3 
      (Batf3) is required for the development of classical CD8alpha+ and CD103+ DCs. By 
      crossing mice deficient in Batf3 with atherosclerosis-prone low density 
      lipoprotein receptor (Ldlr-/-)-deficient mice we here aimed to further address 
      the contribution of Batf3-dependent CD8alpha+ and CD103+ antigen-presenting cells to 
      atherosclerosis. We demonstrate that deficiency in Batf3 entailed mild effects on 
      the immune response in the spleen but did not alter atherosclerotic lesion 
      formation in the aorta or aortic root, nor affected plaque phenotype in low 
      density lipoprotein receptor-deficient mice fed a high fat diet. We thus provide 
      evidence that Batf3-dependent antigen-presenting cells do not have a prominent 
      role in atherosclerosis.
FAU - Gil-Pulido, Jesus
AU  - Gil-Pulido J
AD  - Institute of Experimental Biomedicine, University Hospital Wurzburg, Wurzburg, 
      Germany.
FAU - Cochain, Clement
AU  - Cochain C
AD  - Institute of Experimental Biomedicine, University Hospital Wurzburg, Wurzburg, 
      Germany.
FAU - Lippert, Malte A
AU  - Lippert MA
AD  - Institute of Experimental Biomedicine, University Hospital Wurzburg, Wurzburg, 
      Germany.
FAU - Schneider, Nicole
AU  - Schneider N
AD  - Institute of Experimental Biomedicine, University Hospital Wurzburg, Wurzburg, 
      Germany.
FAU - Butt, Elke
AU  - Butt E
AD  - Institute of Experimental Biomedicine, University Hospital Wurzburg, Wurzburg, 
      Germany.
FAU - Amezaga, Nuria
AU  - Amezaga N
AD  - Institute of Experimental Biomedicine, University Hospital Wurzburg, Wurzburg, 
      Germany.
FAU - Zernecke, Alma
AU  - Zernecke A
AUID- ORCID: 0000-0001-8551-4729
AD  - Institute of Experimental Biomedicine, University Hospital Wurzburg, Wurzburg, 
      Germany.
LA  - eng
PT  - Journal Article
DEP - 20170803
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Basic-Leucine Zipper Transcription Factors)
RN  - 0 (CD8 Antigens)
RN  - 0 (Receptors, LDL)
RN  - 0 (Repressor Proteins)
RN  - 0 (SNFT protein, mouse)
SB  - IM
MH  - Animals
MH  - Antigen Presentation/*immunology
MH  - Basic-Leucine Zipper Transcription Factors/*physiology
MH  - CD8 Antigens/metabolism
MH  - Cells, Cultured
MH  - Dendritic Cells/immunology
MH  - Female
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Plaque, Atherosclerotic/genetics/immunology/*pathology
MH  - Receptors, LDL/*physiology
MH  - Repressor Proteins/*physiology
MH  - Spleen/immunology/metabolism/pathology
MH  - T-Lymphocytes/*immunology
PMC - PMC5542449
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2017/08/05 06:00
MHDA- 2017/10/07 06:00
PMCR- 2017/08/03
CRDT- 2017/08/04 06:00
PHST- 2017/03/31 00:00 [received]
PHST- 2017/07/10 00:00 [accepted]
PHST- 2017/08/04 06:00 [entrez]
PHST- 2017/08/05 06:00 [pubmed]
PHST- 2017/10/07 06:00 [medline]
PHST- 2017/08/03 00:00 [pmc-release]
AID - PONE-D-17-12571 [pii]
AID - 10.1371/journal.pone.0181947 [doi]
PST - epublish
SO  - PLoS One. 2017 Aug 3;12(8):e0181947. doi: 10.1371/journal.pone.0181947. 
      eCollection 2017.