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http://hdl.handle.net/10553/41296
Título: | Cholesterol accumulation in CD11c+ immune cells is a causal and targetable factor in autoimmune disease | Autores/as: | Ito, Ayaka Hong, Cynthia Oka, Kazuhiro Salazar, Jon V. Diehl, Cody Witztum, Joseph L. Díaz-Sarmiento, Mercedes Castrillo Viguera, Antonio Bensinger, Steven J. Chan, Lawrence Tontonoz, Peter |
Clasificación UNESCO: | 32 Ciencias médicas 320710 Inmunopatología |
Palabras clave: | Liver-X-Receptors Apolipoprotein-A-I Systemic-Lupus-Erythematosus B-Cell Rheumatoid-Arthritis, et al. |
Fecha de publicación: | 2016 | Publicación seriada: | Immunity | Resumen: | Liver X receptors (LXRs) are regulators of cholesterol metabolism that also modulate immune responses. Inactivation of LXR alpha and beta 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. LXR beta-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-beta-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/10553/41296 | ISSN: | 1074-7613 | DOI: | 10.1016/j.immuni.2016.11.008 | Fuente: | Immunity [ISSN 1074-7613], v. 45 (6), p. 1311-1326 |
Colección: | Artículos |
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