IVIg-directed DC-platelet nuptials. IVIg effects in autoimmunity and inflammation can be mediated by DCs. IVIg first primes the initiator DCs⁴  in an FcγRIII-dependent manner.^3,5  These cells then propagate a still-poorly described intermediary pathway which may involve the function of several interacting cells. The propagation and/or inhibition stages appear to be dependent on the presence of FcγRIIB and P-selectin. The specific cell that expresses these molecules in terms of IVIg action remains unclear. Platelets have only been thought of as passive victims in ITP, however, Huang et al now show that an important downstream target affected by IVIg-primed DCs could be the platelet rather than the macrophage. A result of this IVIg pathway is the “marking” of the ITP platelet which has reduced ability to engage the phagocytic Mϕ. How the platelet is exactly affected remains unknown but could involve some modification of the platelet or a potential involvement of P-selectin or its ligand PSGL-1. (Professional illustration by Alice Y. Chen.)