RORA and Shock: Using Rorasg/sg, Rorasg/sg bone-marrow chimera (BMC) mice, synthetically blocking the action of RORα, and LysMCreRorafl/sg mice, modeling both ubiquitous and myeloid-cell specific deletion, we demonstrate that RORα can promote recruitment and activation of a myeloid-derived pro-inflammatory macrophage population, which impacts upon the severity and extent of LPS-induced endotoxic shock.