Roszer, TamásMenéndez-Gutiérrez, María PLefterova, Martina IAlameda, DanielNúñez, VanessaLazar, Mitchell AFischer, ThierryRicote, Mercedes2022-11-152022-11-152011-01-01J Immunol . 2011 Jan 1;186(1):621-31.http://hdl.handle.net/20.500.12105/15156Autoimmune glomerulonephritis is a common manifestation of systemic lupus erythematosus (SLE). In this study, we show that mice lacking macrophage expression of the heterodimeric nuclear receptors PPARγ or RXRα develop glomerulonephritis and autoantibodies to nuclear Ags, resembling the nephritis seen in SLE. These mice show deficiencies in phagocytosis and clearance of apoptotic cells, and they are unable to acquire an anti-inflammatory phenotype upon feeding of apoptotic cells, which is critical for the maintenance of self-tolerance. These results demonstrate that stimulation of PPARγ and RXRα in macrophages facilitates apoptotic cell engulfment, and they provide a potential strategy to avoid autoimmunity against dying cells and to attenuate SLE.engVoRhttp://creativecommons.org/licenses/by/4.0/AnimalsAntibodies, AntinuclearApoptosisFemaleLupus NephritisMacrophagesMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicPPAR gammaPhagocytosisRetinoid X Receptor alphaSelf ToleranceAtribución 4.0 Internacional211351661861621-3110.4049/jimmunol.10022301550-6606Journal of immunology (Baltimore, Md. : 1950)open access