During re-infection high-affinity IgG antibodies form complexes with both soluble antigen and antigen displayed on the surface of infected cells. These interactions regulate cellular activation of both innate cells and B cells, which express specific combinations of activating Fc gamma receptors (FcγRI, FcγRIII, FcγRIV) and/or the inhibitory Fc gamma receptor (FcγRIIB). Direct proof for functional expression of FcγR by antigen-specific CD8 T-cells is lacking. Here, we show that the majority of memory CD8 T-cells generated by bacterial or viral infection express only FcγRIIB and that FcγRIIB could be detected on previously activated human CD8 T-cells. Of note, FcγR stimulation during in vivo antigen challenge not only inhibited the cytotoxicity of memory CD8 T-cells against peptide-loaded or virus-infected targets, but FcγRIIB blockade during homologous virus challenge enhanced the secondary CD8 T-cell response. Thus, memory CD8 T-cells intrinsically express a functional FcγRIIB, permitting antigen-antibody complexes to regulate secondary CD8 T-cell responses.