2026-06-14T03:52:15Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/151562024-09-27T08:15:07Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605
Repisalud
author
Roszer, Tamás
author
Menéndez-Gutiérrez, María P
author
Lefterova, Martina I
author
Alameda, Daniel
author
Núñez, Vanessa
author
Lazar, Mitchell A
author
Fischer, Thierry
author
Ricote, Mercedes
funder
Ministerio de Ciencia e Innovación (España)
funder
Fundación Genoma España
funder
Fundación La Marató TV3
funder
Ministerio de Salud (España)
funder
Marie Curie
funder
Fundación ProCNIC
2022-11-15T14:37:35Z
2022-11-15T14:37:35Z
2011-01-01
J Immunol . 2011 Jan 1;186(1):621-31.
10.4049/jimmunol.1002230
1550-6606
Journal of immunology (Baltimore, Md. : 1950)
21135166
http://hdl.handle.net/20.500.12105/15156
Autoimmune 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.
eng
Autoimmune kidney disease and impaired engulfment of apoptotic cells in mice with macrophage peroxisome proliferator-activated receptor gamma or retinoid X receptor alpha deficiency.
journal article
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URL
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J Immunol 2011 Autoimmune Kidney Disease RICOTE.pdf
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J Immunol 2011 Autoimmune Kidney Disease RICOTE.pdf.txt