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Haddad, Yacine; Lahoute, Charlotte; Clément, Marc; Laurans, Ludivine; Metghalchi, Sarvenaz; Zeboudj, Lynda; Giraud, Andreas; Loyer, Xavier; Vandestienne, Marie; Wain-Hobson, Julien; Esposito, Bruno; Potteaux, Stephane; Ait-Oufella, Hafid; Tedgui, Alain; Mallat, Ziad; Taleb, Soraya

The Dendritic Cell Receptor DNGR-1 Promotes the Development of Atherosclerosis in Mice

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  • Medientyp: E-Artikel
  • Titel: The Dendritic Cell Receptor DNGR-1 Promotes the Development of Atherosclerosis in Mice
  • Beteiligte: Haddad, Yacine; Lahoute, Charlotte; Clément, Marc; Laurans, Ludivine; Metghalchi, Sarvenaz; Zeboudj, Lynda; Giraud, Andreas; Loyer, Xavier; Vandestienne, Marie; Wain-Hobson, Julien; Esposito, Bruno; Potteaux, Stephane; Ait-Oufella, Hafid; Tedgui, Alain; Mallat, Ziad; Taleb, Soraya
  • Erschienen: Ovid Technologies (Wolters Kluwer Health), 2017
  • Erschienen in: Circulation Research, 121 (2017) 3, Seite 234-243
  • Sprache: Englisch
  • DOI: 10.1161/circresaha.117.310960
  • ISSN: 0009-7330; 1524-4571
  • Entstehung:
  • Anmerkungen:
  • Beschreibung: Rationale: Necrotic core formation during the development of atherosclerosis is associated with a chronic inflammatory response and promotes accelerated plaque development and instability. However, the molecular links between necrosis and the development of atherosclerosis are not completely understood. Clec9a (C-type lectin receptor) or DNGR-1 (dendritic cell NK lectin group receptor-1) is preferentially expressed by the CD8α + subset of dendritic cells (CD8α + DCs) and is involved in sensing necrotic cells. We hypothesized that sensing of necrotic cells by DNGR-1 plays a determinant role in the inflammatory response of atherosclerosis. Objective: We sought to address the impact of total, bone marrow–restricted, or CD8α + DC–restricted deletion of DNGR-1 on atherosclerosis development. Methods and Results: We show that total absence of DNGR-1 in Apoe (apolipoprotein e)–deficient mice ( Apoe −/− ) and bone marrow–restricted deletion of DNGR-1 in Ldlr (low-density lipoprotein receptor)–deficient mice ( Ldlr −/− ) significantly reduce inflammatory cell content within arterial plaques and limit atherosclerosis development in a context of moderate hypercholesterolemia. This is associated with a significant increase of the expression of interleukin-10 (IL-10). The atheroprotective effect of DNGR-1 deletion is completely abrogated in the absence of bone marrow–derived IL-10. Furthermore, a specific deletion of DNGR-1 in CD8α + DCs significantly increases IL-10 expression, reduces macrophage and T-cell contents within the lesions, and limits the development of atherosclerosis. Conclusions: Our results unravel a new role of DNGR-1 in regulating vascular inflammation and atherosclerosis and potentially identify a new target for disease modulation.
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