IC-mediated activation of DCs upon bindingto FcγR was key for this effect.43 Similarly, in aninfluenza virus infection model, ICs formed with endogenous antiviral antibodies promotedmore sustained antigen presentation by DCs, resulting in stronger CD8+ T-cellproliferation.64 Interestingly, such prolongedantigen presentation by DCs was dependent on virus-specific, isotype-switched antibodiesthat facilitated the capture and cross-presentation of viral antigens by FcγR-expressingDCs. Here, FCGR2A is linked to viral infectious disease.