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Clinical and immunological features of drug-induced and infection-induced proteinase 3-antineutrophil cytoplasmic antibodies and myeloperoxidase-antineutrophil cytoplasmic antibodies and vasculitis

2009; Lippincott Williams & Wilkins; Volume: 22; Issue: 1 Linguagem: Inglês

10.1097/bor.0b013e3283323538

1531-6963

Elena Csernok, Peter Lamprecht, Wolfgang L. Gross,

Neutrophil, Myeloperoxidase and Oxidative Mechanisms

Drugs and infections may induce antineutrophil cytoplasmic antibodies (ANCA) and vasculitic manifestations mimicking ANCA-associated vasculitides (AAV) and mechanisms relevant in their pathogenesis. This review summarizes the most recent findings in this field.Drug-induced and infection-induced proteinase 3 (PR3)-ANCA and myeloperoxidase (MPO)-ANCA may be associated with a vasculitis clinically resembling AAV. Mechanisms relevant for the break of tolerance and induction of ANCA (e.g. danger signals, superantigens, neutrophil extracellular traps, protease-activated receptor-2, IL-17 cells) may be shared to some extent between drug-induced and infection-induced ANCA-positive vasculitis and AAV, especially with regard to the potential role of infection in Wegener's granulomatosis. Differences in immunopathology, clinical presentation, and functional aspects of ANCA help to distinguish drug-induced and infection-induced ANCA-positive vasculitis from AAV, and present new avenues for future research in this field.Medications and infections, which induce PR3-ANCA and MPO-ANCA, have to be considered in the differential diagnosis of primary AAV. Moreover, there is clinical and experimental evidence for an association between certain drugs and infections with ANCA-production. Analysis of ANCA-induction in such conditions also sheds new light on our understanding of immune mechanisms relevant in the break of tolerance and ANCA-production in AAV.