Open AccessDeletion of Batf3-dependent antigen-presenting cells does not affect atherosclerotic lesion formation in mice
Author(s) -
Jesus GilPulido,
Clément Cochain,
Malte A. Lippert,
Nicole Schneider,
Elke Butt,
Núria Amézaga,
Alma Zernecke
Publication year - 2017
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0181947
Subject(s) - immune system , antigen , spleen , immunology , acquired immune system , biology , cross presentation , ldl receptor , cd8 , antigen presentation , phenotype , inflammation , lipoprotein , medicine , t cell , cholesterol , endocrinology , gene , biochemistry
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.