The evolving role of dendritic cells in atherosclerosis

Atherosclerosis, a major contributor to cardiovascular morbidity and mortality, is characterized by chronic inflammation of the arterial wall. This inflammatory process is initiated and maintained by both innate and adaptive immunity. Dendritic cells (DCs), which are antigen-presenting cells, play a...

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Hauptverfasser: Britsch, Simone (VerfasserIn) , Langer, Harald (VerfasserIn) , Dürschmied, Daniel (VerfasserIn) , Becher, Tobias (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: 19 February 2024
In: International journal of molecular sciences
Year: 2024, Jahrgang: 25, Heft: 4, Pages: 1-23
ISSN:1422-0067
DOI:10.3390/ijms25042450
Online-Zugang:Verlag, kostenfrei, Volltext: https://doi.org/10.3390/ijms25042450
Verlag, kostenfrei, Volltext: https://www.mdpi.com/1422-0067/25/4/2450
Volltext
Verfasserangaben:Simone Britsch, Harald Langer, Daniel Duerschmied and Tobias Becher
Beschreibung
Zusammenfassung:Atherosclerosis, a major contributor to cardiovascular morbidity and mortality, is characterized by chronic inflammation of the arterial wall. This inflammatory process is initiated and maintained by both innate and adaptive immunity. Dendritic cells (DCs), which are antigen-presenting cells, play a crucial role in the development of atherosclerosis and consist of various subtypes with distinct functional abilities. Following the recognition and binding of antigens, DCs become potent activators of cellular responses, bridging the innate and adaptive immune systems. The modulation of specific DC subpopulations can have either pro-atherogenic or atheroprotective effects, highlighting the dual pro-inflammatory or tolerogenic roles of DCs. In this work, we provide a comprehensive overview of the evolving roles of DCs and their subtypes in the promotion or limitation of atherosclerosis development. Additionally, we explore antigen pulsing and pharmacological approaches to modulate the function of DCs in the context of atherosclerosis.
Beschreibung:Gesehen am 11.03.2025
Dieser Artikel gehört zum Special issue: Molecular mechanisms and pathophysiology of atherosclerosis 2.0
Beschreibung:Online Resource
ISSN:1422-0067
DOI:10.3390/ijms25042450