On the role of complement and Fc γ-receptors in the Arthus reaction

Jörg Köhl*, J. Engelbert Gessner

*Corresponding author for this work
63 Citations (Scopus)


The contribution of either the complement system or the activation of Fc receptors for IgG (FcγRs) to the inflammatory response in immune complex (IC) disease is puzzling. A series of studies has been performed in mice with engineered deficiencies of either FcγRs, the complement components C3, C4 or the C5a receptor. In addition, different C5-deficient mice strains have been evaluated. Mice with gene targeted disruption of the γ-subunit, which mediates surface expression and signal transduction of the high affinity Fc receptor type I for IgG (FcγRI), the low affinity receptor Fc receptor type III for IgG (FcγRIII) and the high affinity receptor type I for IgE (IgγRI), showed an impaired inflammatory response in the reverse passive Arthus reaction in skin, peritoneum and lung. These data suggest, that the activation of FγRs is the initial event triggering the inflammatory cascade in IC disease. On the other hand, C5aR deficient mice are either protected from tissue injury induced by ICs, as in the lung, or the degree of the inflammatory response is markedly attenuated, as in peritoneum and skin. A detailed analysis of data obtained with the different knock-out strains revealed that both the activation of the complement system as well as the activation of different effector cells via FcγRs contribute to the inflammatory sequelae leading to tissue destruction in IC disease. The relative contributions of FcγRI or FcγRIII and the main effector cells through which these receptors mediate their effector functions are tissue dependent. The activation of the C5a receptor pathway appears to be the prominent contribution of the complement system. (C) 1999 Elsevier Science Ltd.

Original languageEnglish
JournalMolecular Immunology
Issue number13-14
Pages (from-to)893-903
Number of pages11
Publication statusPublished - 01.09.1999


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