Thus, the elimination of influenza-infected cells by the intranasal administration of M2e-based vaccines may be mediated not only by IgG2a/c but also by IgG1 through FcγRIII activation of alveolar macrophages and by sIgA through FcαμR activation of effector cells or by alternative pathways of complement activation. The gene discussed is FCAMR; the disease is influenza.