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Título: | Cholesterol accumulation in CD11c+ immune cells is a causal and targetable factor in autoimmune disease |
Autor: | Ito, Ayaka; Díaz, Mercedes; Castrillo, Antonio CSIC; Bensinger, Steven J.; Tontonoz, Peter | Palabras clave: | LXR Reverse cholesterol transport Autoantibodies Autoimmune diseases |
Fecha de publicación: | 2016 | Editor: | Cell Press Elsevier |
Citación: | Immunity 45(6): 1311-1326 (2016) | Resumen: | 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. | URI: | http://hdl.handle.net/10261/151124 | DOI: | 10.1016/j.immuni.2016.11.008 | Identificadores: | doi: 10.1016/j.immuni.2016.11.008 e-issn: 1097-4180 issn: 1074-7613 |
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