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RI/III and C5aR in the Reverse Arthus Reaction1
*
Department of Clinical Immunology,
Institute of Medical Microbiology, and
Department of Functional Anatomy, Medical School Hannover, Hannover, Germany; and
Department of Human and Clinical Genetics, Leiden University Medical Center, Leiden, The Netherlands
Recent attempts to specify the relative contribution of FcR and
complement in various experimental systems of immune complex disease
have led to opposing conclusions. As concluded in IgG
FcR
-/- mice, manifestation of disease is almost
exclusively determined by FcR on effector cells, arguing for a minor
role of complement. In contrast, data obtained with
C5aR-/- mice suggested that, dependent on the tissue
site, complement is more important than FcR. In this paper, we
demonstrate that, in response to IgG immune complex formation,
FcRI/III- and C5aR-mediated pathways are both necessary and only
together are they sufficient to trigger the full expression of
inflammation in skin and lung. Moreover, both effector systems are not
entirely independent, suggesting an interaction between FcR and
C5aR. Therefore, FcR-mediated responses can be integrated through
C5aR activation, which may explain why these two receptor pathways have
previously been considered to dominate each
other.
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