We focused on this activating FcγR because of its restricted expression on macrophages, monocytes, neutrophils and dendritic cells but no other myeloid cell population, and because of its very high affinity for IgG2a monoclonal antibodies, which contribute the most protection by non-neutralizing influenza antibodies in the mouse model (13, 20). This evidence concerns the gene FCGR2A and influenza.