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Published online before print May 22, 2003
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Department of Internal Medicine, University Hospital Groningen, The Netherlands
Correspondence: Prof. Dr. C. G. M. Kallenberg, Department of Internal Medicine, University Hospital Groningen, Hanzeplein 1, 9713 GZ Groningen, The Netherlands. E-mail: c.g.m.kallenberg{at}int.azg.nl
Accumulating in vivo and in vitro evidence supports the hypothesis that antineutrophil cytoplasm autoantibodies (ANCA) with specificity for proteinase 3 (PR3) and myeloperoxidase (MPO) are involved in the pathophysiology of small-vessel vasculitis. The best-described effector function of these autoantibodies is stimulation of neutrophils to produce reactive oxygen species and to release proteolytic enzymes. Neutrophil activation requires interaction of monomeric ANCA with PR3/MPO and Fc
receptors, but also other mechanisms—for instance, stimulation by ANCA-containing immune complexes—cannot be excluded. This review focuses on the mechanisms of neutrophil activation by ANCA. We discuss the molecules involved in ANCA binding to the neutrophil surface and in triggering the functional responses. We summarize current knowledge on the signal-transduction pathways initiated by ANCA and on the factors determining susceptibility of neutrophils to activation by these autoantibodies.
Key Words: ANCA • proteinase 3 • myeloperoxidase • Fc receptors • oxidative burst
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