Neutrophils promote 6-sulfo LacNAc+ dendritic cell (slanDC) survival.

There is increasing evidence supporting the notion that neutrophils and other leukocytes establish cooperative actions in regulating innate and adaptive immune responses. In such a context, we have shown recently that human neutrophils amplify NK cell/slanDC-mediated cytokine production by directly costimulating IFN-γ production by NK cells, as well as by potentiating IL-12p70 release by slanDCs via CD18/ICAM-1 interactions. To gain more insights into the molecular bases of the neutrophil-mediated cytokine potentiation by NK cells and slanDCs under coculture conditions, we now report that neutrophils efficaciously maintain slanDC survival by contact-dependent mechanisms. Such a phenomenon occurs in the absence or presence of NK cells, which, in the presence of LPS and IL-2 or the IL-15/IL-18 combination, accelerates slanDC apoptosis significantly. Noteworthy, αICAM-1- and αCD18-neutralizing antibodies, previously shown to suppress IL-12p70 production by slanDCs and consequently, IFN-γ by NK cells under similar experimental conditions, did not minimally alter the neutrophil-mediated prosurvival effect on slanDCs. Altogether, data not only expand our knowledge on the interactions between human neutrophils and slanDCs but also prove that neutrophil-mediated promotion of slanDC survival and potentiation of slanDC-derived IL-12p70 occur via different mechanisms.