Deletion of Batf3-dependent antigen-presenting cells does not affect atherosclerotic lesion formation in mice.

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 cyto...

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Main Authors: Jesus Gil-Pulido, Clement Cochain, Malte A Lippert, Nicole Schneider, Elke Butt, Núria Amézaga, Alma Zernecke
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2017-01-01
Series:PLoS ONE
Online Access:https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0181947&type=printable
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author Jesus Gil-Pulido
Clement Cochain
Malte A Lippert
Nicole Schneider
Elke Butt
Núria Amézaga
Alma Zernecke
author_facet Jesus Gil-Pulido
Clement Cochain
Malte A Lippert
Nicole Schneider
Elke Butt
Núria Amézaga
Alma Zernecke
author_sort Jesus Gil-Pulido
collection DOAJ
description 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.
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publisher Public Library of Science (PLoS)
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spelling doaj-art-4ba99e53a63b43899bb55b41046166a32025-08-20T02:03:59ZengPublic Library of Science (PLoS)PLoS ONE1932-62032017-01-01128e018194710.1371/journal.pone.0181947Deletion of Batf3-dependent antigen-presenting cells does not affect atherosclerotic lesion formation in mice.Jesus Gil-PulidoClement CochainMalte A LippertNicole SchneiderElke ButtNúria AmézagaAlma ZerneckeAtherosclerosis 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.https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0181947&type=printable
spellingShingle Jesus Gil-Pulido
Clement Cochain
Malte A Lippert
Nicole Schneider
Elke Butt
Núria Amézaga
Alma Zernecke
Deletion of Batf3-dependent antigen-presenting cells does not affect atherosclerotic lesion formation in mice.
PLoS ONE
title Deletion of Batf3-dependent antigen-presenting cells does not affect atherosclerotic lesion formation in mice.
title_full Deletion of Batf3-dependent antigen-presenting cells does not affect atherosclerotic lesion formation in mice.
title_fullStr Deletion of Batf3-dependent antigen-presenting cells does not affect atherosclerotic lesion formation in mice.
title_full_unstemmed Deletion of Batf3-dependent antigen-presenting cells does not affect atherosclerotic lesion formation in mice.
title_short Deletion of Batf3-dependent antigen-presenting cells does not affect atherosclerotic lesion formation in mice.
title_sort deletion of batf3 dependent antigen presenting cells does not affect atherosclerotic lesion formation in mice
url https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0181947&type=printable
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