Modulation of macrophage efferocytosis in inflammation.

摘要: A critical function of macrophages within the inflammatory milieu is removal dying cells by a specialized phagocytic process called efferocytosis (“to carry to grave”). Through specific receptor engagement and induction downstream signaling, efferocytosing promote resolution inflammation (i) efficiently engulfing cells, thus avoiding cellular disruption release contents, (ii) producing anti-inflammatory mediators such as IL-10 TGF-β that dampen pro-inflammatory responses. Evidence suggests plasticity in macrophage programming, response changing environmental cues, modulates efferocytic capability. Essential programming for enhanced activation nuclear receptors PPARγ, PPARδ, LXR, possibly RXRα. Additionally, number signals milieu, including those from themselves, can influence efficacy either acting immediate inhibitors/enhancers or altering longer-term effects. Importantly, sustained lead defective apoptotic cell clearance associated with development autoimmunity other chronic disorders. This review summarizes current knowledge multiple factors modulate ability highlights emerging therapeutic targets significant potential limiting inflammation.