Send to

Choose Destination

See 1 citation found by title matching your search:

Immunity. 2016 Dec 20;45(6):1311-1326. doi: 10.1016/j.immuni.2016.11.008.

Cholesterol Accumulation in CD11c+ Immune Cells Is a Causal and Targetable Factor in Autoimmune Disease.

Author information

Department of Pathology and Laboratory Medicine, University of California, Los Angeles, CA 90095, USA.
Departments of Medicine, Molecular & Cellular Biology and Biochemistry, Baylor College of Medicine, 1 Baylor Plaza, Houston, TX 77030, USA.
Department of Medicine, University of California, San Diego, CA 92037, USA.
Instituto de Investigaciones Biomédicas "Alberto Sols" Madrid, Consejo Superior de Investigaciones Cientificas y Unidad de Biomedicina (Unidad Asociada al CSIC), Instituto Universitario de Investigaciones Biomedicas y Sanitarias (IUIBS), Universidad de las Palmas de Gran Canaria, Las Palmas, Spain.
Department of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, CA 90095, USA.
Department of Pathology and Laboratory Medicine, University of California, Los Angeles, CA 90095, USA; Howard Hughes Medical Institute, University of California, Los Angeles, CA 90095, USA. Electronic address:


Liver X receptors (LXRs) are regulators of cholesterol metabolism that also modulate immune responses. Inactivation of LXR α and β in mice leads to autoimmunity; however, how the regulation of cholesterol metabolism contributes to autoimmunity is unclear. Here we found that cholesterol loading of CD11c+ cells triggered the development of autoimmunity, whereas preventing excess lipid accumulation by promoting cholesterol efflux was therapeutic. LXRβ-deficient mice crossed to the hyperlipidemic ApoE-deficient background or challenged with a high-cholesterol diet developed autoantibodies. Cholesterol accumulation in lymphoid organs promoted T cell priming and stimulated the production of the B cell growth factors Baff and April. Conversely, B cell expansion and the development of autoantibodies in ApoE/LXR-β-deficient mice was reversed by ApoA-I expression. These findings implicate cholesterol imbalance as a contributor to immune dysfunction and suggest that stimulating HDL-dependent reverse cholesterol transport could be beneficial in the setting of autoimmune disease.


LXR; autoantibodies; autoimmune disease; reverse cholesterol transport

[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center