Cutting edge: Fc receptor type I for IgG on macrophages and complement mediate the inflammatory response in immune complex peritonitis

The contributions of Fc receptors (FcRs) for IgG (FcγRs) and complement to immune complex (IC)-mediated peritonitis were evaluated in BALB/c-, C57BL/6-, FcRγ, chain-, and FcR type III for IgG (FcγRIII)-deficient mice, backcrossed to the C57BL/6 background. In BALB/c mice, but not in C57BL/6 mice, neutrophil migration was markedly attenuated after complement depletion. In mice lacking FcRγ, chain, nentrophil migration was abolished, whereas it was unaffected in FcγRIII-deficient mice. Huge amounts of TNF-α (TNF) were found in the peritoneal exudate of BALB/c and C57BL/6 mice but were absent in mice lacking FcRγ chain or FcγRIII. Surprisingly, a functional inhibition of TNF in BALB/c and C57BL/6 mice had no effect on neutrophil infiltration. These data provide evidence that in IC peritonitis, the activation of FcR type I for IgG on peritoneal macrophages and the activation of the complement cascade, but not the interaction of ICs with FcγRIII and the subsequent release of TNF, initiate the inflammatory response in BALB/c and C57BL/6 mice.