Priming of Human Resting NK Cells by Autologous M1 Macrophages via the Engagement of IL-1β, IFN-β, and IL-15 Pathways

摘要: The cross talk between NK cells and macrophages is emerging as a major line of defense against microbial infections tumors. This study reveals complex network soluble mediators cell-to-cell interactions allowing human classically activated (M1) macrophages, but not resting (M0) or alternatively (M2) to prime autologous cells. In this article, we show that M1 increase cell cytotoxicity by IL-23 IFN-β-dependent upregulation NKG2D, IL-1β-dependent NKp44, trans-presentation IL-15. Moreover, both cis-presentation IL-15 on engagement the 2B4-CD48 pathway are used trigger production IFN-γ. disclosure these synergic cellular mechanisms regulating M1-NK provides novel insights better understand role innate immune responses in physiopathology tumor biology infections.