Jon Salazar

TL;DR: It is found that liver X receptor (LXR) signaling was important for both apoptotic cell clearance and the maintenance of immune tolerance and treatment with an LXR agonist ameliorated disease progression in a mouse model of lupus-like autoimmunity.

TL;DR: It is found that cholesterol loading of CD11c+ cells triggered the development of autoimmunity, whereas preventing excess lipid accumulation by promoting cholesterol efflux was therapeutic, and stimulating HDL-dependent reverse cholesterol transport could be beneficial in the setting of autoimmune disease.

TL;DR: An LXR gain-of-function system that does not depend on the addition of exogenous ligand is described and it is shown that the ARL7 promoter contains a functional LXRE and can be transactivated by LXRs in a sequence-specific manner, indicating that ARL 7 is a direct target of LXR.

TL;DR: The results do not exclude a contribution of macrophage PPAR and LXR expression to systemic metabolism in certain contexts, but these factors do not appear to be dominant contributors to glucose tolerance in a high-fat-fed Th1-biased bone marrow transplant model.

TL;DR: A previously unrecognized requirement for hepatic LXR α for optimal reverse cholesterol transport in mice is revealed, linked to a specific requirement for LXRα−/− in the expression of hepatic NXR target genes involved in sterol transport and metabolism.