Apolipoprotein E derived from CD11c+ cells ameliorates atherosclerosis

Manuela Sauter, Reinhard J. Sauter, Henry Nording, Chaolan Lin, Marcus Olbrich, Stella Autenrieth, Christian Gleissner, Martin Thunemann, Nadia Otero, Esther Lutgens, Zouhair Aherrahrou, Dennis Wolf, Lars Zender, Sven Meuth, Robert Feil, Harald F. Langer

Research output: Contribution to journalArticlepeer-review


Atherosclerosis is studied in models with dysfunctional lipid homeostasis—predominantly the ApoE−/− mouse. The role of antigen-presenting cells (APCs) for lipid homeostasis is not clear. Using a LacZ reporter mouse, we showed that CD11c+ cells were enriched in aortae of ApoE−/− mice. Systemic long-term depletion of CD11c+ cells in ApoE−/− mice resulted in significantly increased plaque formation associated with reduced serum ApoE levels. In CD11ccre+ApoEfl/fl and Albumincre+ApoEfl/fl mice, we could show that ≈70% of ApoE is liver-derived and ≈25% originates from CD11c+ cells associated with significantly increased atherosclerotic plaque burden in both strains. Exposure to acLDL promoted cholesterol efflux from CD11c+ cells and cell-specific deletion of ApoE resulted in increased inflammation reflected by increased IL-1β serum levels. Our results determined for the first time the level of ApoE originating from CD11c+ cells and demonstrated that CD11c+ cells ameliorate atherosclerosis by the secretion of ApoE.

Original languageEnglish (US)
Article number103677
Issue number1
StatePublished - Jan 21 2022


  • Biological sciences
  • Components of the immune system
  • Immune response
  • Molecular biology

ASJC Scopus subject areas

  • General


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