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 dendritic cells (moDCs) with similar efficiency as allogeneic apoptotic neutrophils [Majai G et al. (2010) J Leukoc Biol 88, 981-991]. Interestingly, in contrast to the allogeneic system, exposure of moDCs to autologous apoptotic neutrophils inhibits LPS + IFN-γ-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 IFN-γ-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, and allow increased clearance of dying cells by macrophages.