Immune complex initiation of inflammatory diseases is mediated, to a large extent, by Fcgamma receptors. Recent data have underscored three essential points: (1) there is substantial structural diversity within three distinct families of Fcgamma receptors; (2) there are functionally significant alleles of different receptor isoforms; and (3) each cell type has a unique distribution of Fcgamma receptor isoforms. Structurally different Fcgamma receptors utilize distinct signal transduction pathways. Thus, in clinical immune complex disease, consideration of the predominant cell type and receptor isoform involved, as well as the genotype of the individual patient, will be important in developing and applying targeted downregulatory agents such as misoprostol.