Figure 1

The two primary forms of interaction between therapeutic IgGs and FcγRs. On the left: when IgG is bound to high levels of antigen on target cells, such as tumor cells, the resulting clustered Fc domains engage with FcγRs on immune effector cells such as NK cells and macrophages. This drives signals through those FcγRs triggering the initiation of cell-mediated effector functions such as ADCC and ADCP. On the right: when IgG is bound by its Fc domain to FcγRs it can act to cluster low levels of target receptors, such as members of the TNFR family. This clustering acts to trigger signals though the TNFR into target cells, such as T cells.