By Richard A. DeRemee (auth.), Wolfgang L. Gross (eds.)

Preface: Pathophysiological Athophysiological features and Antigen Specificity: cANCA-Targets. Proteinase three and so forth. pANCA-Targets: a. Myeloperoxidase. pANCA-Targets: b. different Lysosomal Antigens. ANCA-Targets: Endothelial mobilephone components. Animal reviews and Animal versions. medical elements of Wegener's Granulomatosis and different ANCA linked illnesses: Wegener's and ANCA linked Vasculitis. healing techniques. ANCA and Inflamatory Bowel and Liver illnesses: Gastroenterologic features. a hundred articles. Index.

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Extra info for ANCA-Associated Vasculitides: Immunological and Clinical Aspects

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A. Thompson, Endothelium, myeloperoxidase, anti-myeloperoxidase interaction in vasculitis. Abstract in the Proceedings ofthe 4th International Workshop on ANCA. Advances in Experimental Medicine and Biology, Plenum Press, London (1993) 4. J. Mayet, E. Hermann, E. Csemok, et al, In vitro interactions of C-ANCA (antibodies to proteinase 3) with human endothelial cells. Abstract in the Proceedings ofthe 4th International Workshop on ANCA. Advances in Experimental Medicine and Biology, Plenum Press, London (1993) 5.

Spontaneously hypertensive rats with either circulating radiolabeled albumin or circulating chromium-labeled neutrophils received intradermal injections of anti-MPO IgG (or F(ab')2 lgG) or control IgG, with or without a prin1er. Assay for radiolabeled albumin in the skin demonstrated increased vascular permeability that was optimum with prin1er plus anti-MPO. F(ab')2 anti-MPO IgG was also capable of inducing increased vascular permeability. Assay for chromium in the skin indicated that there was an accumulation of neutrophils at the site of anti-MPO IgG injection which was not caused by control IgG.

Exacerbations of Wegener's granulomatosis are known to frequently follow viral or bacterial respiratory tract infectionsl7, and over 90% of patients with ANCAassociated vasculitis give a history of flu-like symptoms soon before the onset of vasculitic manifestationsl8. It is possible that this relationship between infection and ANCA-associated vasculitis is a clinical manifestation of the link between neutrophil (and monocyte) priming and ANCA-induced activation. No matter how attractive the current hypotheses are, however, the available data are inadequate to conclude that ANCA are directly involved in the pathogenesis of ANCA-associated vasculitis.

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