Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/44416
Title: Apoptotic Cells Promote Their Own Clearance and Immune Tolerance through Activation of the Nuclear Receptor LXR
Authors: A-Gonzalez, Noelia
Bensinger, Steven J.
Hong, Cynthia
Beceiro Casas, Susana 
Bradley, Michelle N.
Zelcer, Noam
Deniz, Jose
Ramirez, Cristina
Díaz, Mercedes 
Gallardo Campos, Germán 
Ruiz de Galarreta, Carlos
Salazar, Jon
López Blanco, Félix 
Edwards, Peter
Parks, John
Andujar, Miguel 
Tontonoz, Peter
Castrillo Viguera, Antonio Jesús 
UNESCO Clasification: 32 Ciencias médicas
Keywords: Liver-X-Receptors
Mer Tyrosine Kinase
Mice Lacking
Phosphatidylserine Receptor
Signaling Pathways, et al
Issue Date: 2009
Publisher: 1074-7613
Project: Saf2005-03270. Los Receptores Lxr y Su Papel en la Respuesta Inflamatoria, Inmunitaria y Apoptótica. 
Journal: Immunity 
Abstract: Effective clearance of apoptotic cells by macrophages is essential for immune homeostasis. The transcriptional pathways that allow macrophages to sense and respond to apoptotic cells are poorly defined. We demonstrate here that LXR signaling is important for both apoptotic cell clearance and the maintenance of immune tolerance. Apoptotic cell engulfment activates LXR and thereby induces the expression of Mer, a receptor tyrosine kinase critical for phagocytosis. LXR null macrophages exhibit a selective defect in phagocytosis of apoptotic cells and an aberrant pro-inflammatory response to them. As a consequence of these defects, mice lacking LXRs manifest a breakdown in self-tolerance and develop autoantibodies and autoimmune glomerulonephritis. Treatment with an LXR agonist ameliorates disease progression in mouse models of Lupus-like autoimmunity. Thus, activation of LXR by apoptotic cells engages a virtuous cycle that promotes their own clearance and couples engulfment to the suppression of inflammatory pathways.
URI: http://hdl.handle.net/10553/44416
ISSN: 1074-7613
DOI: 10.1016/j.immuni.2009.06.018
Source: Immunity [ISSN 1074-7613], v. 31, p. 245-258
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