Autologous apoptotic neutrophils inhibit inflammatory cytokine secretion by human dendritic cells, but enhance Th1 responses.

Neutrophils represent the most abundant cell type in peripheral blood, and exhibit a remarkably brief (6-8 h) half-life in circulation. The fundamental role of these professional phagocytes has been established in acute inflammation, based on their potential to both initiate and receive inflammatory signals. Furthermore, neutrophils also take part in maintaining chronic inflammatory processes, such as in various autoimmune diseases. Here we demonstrate that human autologous apoptotic neutrophils are readily engulfed by immature monocyte-derived DCs (moDCs) with similar efficiency as allogeneic apoptotic neutrophils [1]. Interestingly, in contrast to the allogeneic system, exposure of moDCs to autologous apoptotic neutrophils inhibits LPS+IFNγ-induced production of inflammatory cytokines in a phagocytosis independent manner. Autologous apoptotic neutrophil-primed DCs are able to modulate T-cell responses by inducing the generation of IFNγ-secreting cells while hampering that of IL-17A-producing cells. Our observations indicate that capture of autologous apoptotic neutrophils by immature DCs may impede further neutrophil-mediated phagocytosis and tissue damage, as well as allow increased clearance of dying cells by macrophages.