Deletion of Batf3-dependent antigen-presenting cells does not affect atherosclerotic lesion formation in mice
Zitieren Sie bitte immer diese URN: urn:nbn:de:bvb:20-opus-170535
- 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\(^{+}\) andAtherosclerosis 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.…
Autor(en): | Jesus Gil-Pulido, Clement Cochain, Malte A. Lippert, Nicole Schneider, Elke Butt, Núria Amézaga, Alma Zernecke |
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URN: | urn:nbn:de:bvb:20-opus-170535 |
Dokumentart: | Artikel / Aufsatz in einer Zeitschrift |
Institute der Universität: | Medizinische Fakultät / Institut für Experimentelle Biomedizin |
Sprache der Veröffentlichung: | Englisch |
Titel des übergeordneten Werkes / der Zeitschrift (Englisch): | PLoS ONE |
Erscheinungsjahr: | 2017 |
Band / Jahrgang: | 12 |
Heft / Ausgabe: | 8 |
Seitenangabe: | e0181947 |
Originalveröffentlichung / Quelle: | PLoS ONE 12(8):e0181947 (2017). DOI: 10.1371/journal.pone.0181947 |
DOI: | https://doi.org/10.1371/journal.pone.0181947 |
PubMed-ID: | https://pubmed.ncbi.nlm.nih.gov/28771609 |
Allgemeine fachliche Zuordnung (DDC-Klassifikation): | 6 Technik, Medizin, angewandte Wissenschaften / 61 Medizin und Gesundheit / 610 Medizin und Gesundheit |
Freie Schlagwort(e): | Batf3; atherosclerosis; deficiency; dendritic cells |
Datum der Freischaltung: | 27.09.2019 |
Lizenz (Deutsch): | CC BY: Creative-Commons-Lizenz: Namensnennung 4.0 International |