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Pathophysiology of ANCA-associated small vessel vasculitis Kallenberg CGCurr Rheumatol Rep 2010[Dec]; 12 (6): 399-405Antineutrophil cytoplasmic autoantibodies (ANCAs) directed to proteinase 3 (PR3-ANCA) or myeloperoxidase (MPO-ANCA) are strongly associated with the ANCA-associated vasculitides--Wegener's granulomatosis, microscopic polyangiitis, and Churg-Strauss syndrome. Clinical observations, including the efficacy of B-cell depletion via rituximab treatment, support--but do not prove--a pathogenic role for ANCA in the ANCA-associated vasculitides. In vitro experimental studies show that the interplay of ANCA, neutrophils, the alternative pathway of the complement system, and endothelial cells could result in lysis of the endothelium. A pathogenic role for MPO-ANCA is strongly supported by in vivo experimental studies in mice and rats, which also elucidate the pathogenic mechanisms involved in lesion development. Unfortunately, an animal model for PR3-ANCA-associated Wegener's granulomatosis is not yet available. Here, cellular immunity appears to play a major role as well, particularly via interleukin-17-producing T cells, in line with granulomatous inflammation in the lesions. Finally, microbial factors, in particular Staphylococcus aureus and gram-negative bacteria, seem to be involved in disease induction and expression, but further studies are needed to define their precise role in disease development.|Animals[MESH]|Antibodies, Antineutrophil Cytoplasmic/*blood[MESH]|Cells, Cultured[MESH]|Disease Models, Animal[MESH]|Humans[MESH]|Immunity, Cellular/immunology[MESH]|Mice[MESH]|Microscopic Polyangiitis/immunology/pathology/*physiopathology[MESH]|Myeloblastin/immunology[MESH]|Neutrophils/cytology/immunology[MESH]|Peroxidase/immunology[MESH]|Rats[MESH]|Staphylococcus aureus/immunology/pathogenicity[MESH]|Th17 Cells/immunology[MESH] |
