Immune complexes have been shown to activate the complement system leading to the generation of C5a in this peritonitis model, which then initiates the inflammatory cascade - both through direct C5aR-mediated effector functions on infiltrating and resident cells, and, also indirectly, by shifting the balance between activating (FcγRI and FcγRIII) and inhibitory (FcγRIIB) Fcγ receptors on resident cells toward an inflammatory phenotype [20]; also, ablation of C5aR signaling abrogates neutrophil recruitment and production of KC and MIP-2 in the same model [20]. This evidence concerns the gene FCGR2B and peritonitis.