Inhibition of phagocytosis in vivo can be accomplished via IC-mediated inhibition of FcγR functional activity. These complexes, varying in size and valency, operate through distinct mechanistic pathways. IVIg leads to the formation of variably sized ICs, including small monomeric and dimeric complexes. The small ICs (Ig dimers or soluble antigen/donor Ig complexes) require CSF-1–dependent macrophages and FcγRII expression to mediate their as-yet-undefined anti-inflammatory effect. Intravenous anti-D generates large particulate ICs, namely opsonized rbcs. These large ICs induce a phagocytic block in vivo in a manner independent of FcγRII expression. Perhaps mimicking the situation directly, antibodies that specifically engage either the inhibitory FcγRII (4) or the activating FcγRIII (4, 5) can also induce platelet count recovery.