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Antineutrophil cytoplasmic antibody (ANCA) vasculitis is characterised by autoantibodies against myeloperoxidase (MPO) and proteinase 3 (PR3). The evidence that ANCA are pathogenic comes from in vitro studies in which IgG from patients with anti-MPO or anti-PR3 antibodies activate neutrophils to undergo respiratory burst and degranulation. Furthermore, murine monoclonal antibodies against human MPO and PR3 and a chimeric humanised anti-PR3 monoclonal antibody activate neutrophils. The paradigm of neutrophil activation by ANCA has therefore become established.1 Further support for the pathogenicity of ANCA comes from in vivo studies in which injection of anti-MPO antibodies causes focal necrotising crescentic glomerulonephritis in mice.2
We assessed the effect of purified ANCA on the activation of TNFα primed neutrophils using 10 control IgGs, 11 MPO-ANCA and 9 PR3-ANCA using two different assays of the neutrophil respiratory burst (full methods are in a online supplementary file 1). We found no significant difference in two separate neutrophil donors (figure 1A-C). We also used assays for four markers of neutrophil degranulation and found no differences in two neutrophil donors (figure 1D-G). The results are not due to inactivity of the purified ANCA IgG preparations. Aliquots of the same ANCA and control IgG batches were used in a recent …
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