TY  - JOUR
A1  - Gil-Pulido, Jesus
A1  - Cochain, Clement
A1  - Lippert, Malte A.
A1  - Schneider, Nicole
A1  - Butt, Elke
A1  - Amézaga, Núria
A1  - Zernecke, Alma
T1  - Deletion of Batf3-dependent antigen-presenting cells does not affect atherosclerotic lesion formation in mice
JF  - PLoS ONE
N2  - 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 CD8α\(^{+}\) 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 CD8α\(^{+}\) 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.
KW  - atherosclerosis
KW  - dendritic cells
KW  - Batf3
KW  - deficiency
Y1  - 2017
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-170535
VL  - 12
IS  - 8
ER  -