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 (Fc gamma Rs) and compleme nt to immune complex (IC)-mediated peritonitis were evaluated in BALB/c-, C 57BL/6-, FcR gamma chain-, and FcR type III for IgG (Fc gamma RIII)-deficie nt 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 FcR gamma chain, neutrophil migration was aboli shed, whereas it was unaffected in Fc gamma RIII-deficient mice. Huge amoun ts of TNF-alpha (TNF) were found in the peritoneal exudate of BALB/c and C5 7BL/6 mice but were absent in mice lacking FcR gamma chain or Fc gamma RIII , Surprisingly, a functional inhibition of TNF in BALB/c and C57BL/6 mice h ad no effect on neutrophil infiltration. These data provide evidence that i n IC peritonitis, the activation of FcR type I for IgG on peritoneal macrop hages and the activation of the complement cascade, but not the interaction of ICs with Fc gamma RIII and the subsequent release of TNF, initiate the inflammatory response in BALB/c and C57BL/6 mice.