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Assessment of Human Natural Killer Cell Events Driven by FcγRIIIa Engagement in the Presence of Therapeutic Antibodies
Published on: May 22, 2020
Mechanism of human natural killer cell activation by Haemophilus ducreyi
Wei Li1, Diane M Janowicz, Kate R Fortney
1Department of Medicine, Center for Immunobiology, School of Medicine, Indiana University, Indianapolis, Indiana 46202, USA. wl1@iupui.edu
The role of natural killer (NK) cells in the host response to Haemophilus ducreyi infection is unclear. In pustules obtained from infected human volunteers, there was an enrichment of CD56bright NK cells bearing the activation markers CD69 and HLA-DR, compared with peripheral blood. To study the mechanism by which H. ducreyi activated NK cells, we used peripheral blood mononuclear cells from uninfected volunteers. H. ducreyi activated NK cells only in the presence of antigen-presenting cells. H. ducreyi-infected monocytes and monocyte-derived macrophages activated NK cells in a contact- and interleukin-18 (IL-18)-dependent manner, whereas monocyte-derived dendritic cells induced NK activation through soluble IL-12. More lesional NK cells than peripheral blood NK cells produced IFN-gamma in response to IL-12 and IL-18. We conclude that NK cells are recruited to experimental lesions and likely are activated by infected macrophages and dendritic cells. IFN-gamma produced by lesional NK cells may facilitate phagocytosis of H. ducreyi.
The role of natural killer (NK) cells in the host response to Haemophilus ducreyi infection is unclear. In pustules obtained from infected human volunteers, there was an enrichment of CD56bright NK cells bearing the activation markers CD69 and HLA-DR, compared with peripheral blood. To study the mechanism by which H. ducreyi activated NK cells, we used peripheral blood mononuclear cells from uninfected volunteers. H. ducreyi activated NK cells only in the presence of antigen-presenting cells. H. ducreyi-infected monocytes and monocyte-derived macrophages activated NK cells in a contact- and interleukin-18 (IL-18)-dependent manner, whereas monocyte-derived dendritic cells induced NK activation through soluble IL-12. More lesional NK cells than peripheral blood NK cells produced IFN-gamma in response to IL-12 and IL-18. We conclude that NK cells are recruited to experimental lesions and likely are activated by infected macrophages and dendritic cells. IFN-gamma produced by lesional NK cells may facilitate phagocytosis of H. ducreyi.
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