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CUTTING EDGE |
*
Institute of Medical Microbiology, and
Department of Clinical Immunology, Medical School Hannover, Hannover, Germany
The contributions of Fc receptors (FcRs) for
IgG (Fc
Rs) and complement to immune complex (IC)-mediated
peritonitis were evaluated in BALB/c-, C57BL/6-, FcR chain-, and FcR
type III for IgG (FcRIII)-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 FcR chain, neutrophil migration was abolished, whereas it
was unaffected in FcRIII-deficient mice. Huge amounts of TNF-
(TNF) were found in the peritoneal exudate of BALB/c and C57BL/6 mice
but were absent in mice lacking FcR chain or FcRIII.
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 FcRIII and the subsequent
release of TNF, initiate the inflammatory response in BALB/c and
C57BL/6 mice.
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