vasculitis/protease

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Immunologic vasculitis in beige mice with deficiency of leukocytic neutral protease.

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Immune complex vasculitis has been induced in normal mice and in mice with features of the Chediak-Higashi syndrome ("beige" mice). The accumulation of neutrophils in peritoneal exudates after the injection of C5a is not quantitatively depressed in beige as compared with normal mice. Immune

Occurrence of antibodies to protease-treated histones in a patient with vasculitis.

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We describe the presence of IgG antibodies reacting with histones previously treated with proteases in a patient with vasculitis. The patient's serum did not react with nontreated histones and when several enzymes were tested separately, only alpha-chymotrypsin reproduced the effect. Reactivity was

PegIFNα/ribavirin/protease inhibitor combination in severe hepatitis C virus-associated mixed cryoglobulinemia vasculitis.

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OBJECTIVE The aim of this study was to analyse the safety and efficacy of the PegIFNα/ribavirin/protease inhibitor combination in severe and/or refractory hepatitis C virus (HCV)-mixed cryoglobulinemia (MC) vasculitis. METHODS This prospective cohort study included 30 patients (median age 59 years

Peg-IFNα/ribavirin/protease inhibitor combination in hepatitis C virus associated mixed cryoglobulinemia vasculitis: results at week 24.

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BACKGROUND The standard-of-care treatment of patients with hepatitis C virus (HCV)-mixed cryoglobulinemia (MC) vasculitis includes pegylated interferon α (PegIFN)-α plus ribavirin and/or rituximab. About 30-40% of patients are non-responders or relapsers to such combination. OBJECTIVE To analyse the

Alpha-1-antitrypsin phenotyping in ANCA-associated diseases: one of several arguments for protease/antiprotease imbalance in systemic vasculitis.

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The vasculitic lesions observed in Wegener's granulomatosis may be partly the consequence of proteases released following activation of neutrophils by ANCA. The activity of these proteases, including proteinase 3 (PR3) and elastase, is normally closely restricted to the inflammation site by a large

Effective treatment with alpha 1-protease inhibitor of chronic cutaneous vasculitis associated with alpha 1-antitrypsin deficiency.

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The primary serum proteinase inhibitor is alpha 1-antitrypsin, and deficiency of this enzyme has been associated with a variety of systemic and cutaneous disorders. We report cutaneous vasculitis in a 49-year-old man with alpha 1-antitrypsin deficiency. His condition persisted despite treatment with

Cytokines, growth factors and proteases in medium and large vessel vasculitis.

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Giant cell arteritis and Takayasu arteritis are autoimmune vasculitides that cause aneurysm formation and tissue infarction. Extravascular inflammation consists of an intense acute phase response. Deeper understanding of pathogenic events in the vessel wall has highlighted the loss of tissue

Platelets are activated in ANCA-associated vasculitis via thrombin-PARs pathway and can activate the alternative complement pathway.

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BACKGROUND In this study, we investigated the mechanism of platelet activation in patients with antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV), as well as the activation of the alternative complement pathway by platelets in AAV. METHODS CD62P and platelet-leukocyte aggregates

Immune complexes in sera from patients with rheumatoid vasculitis induce polymorphonuclear cell-mediated injury to endothelial cells.

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The ability of sera from 11 patients with rheumatoid arthritis (RA) complicated by leukocytoclastic vasculitis (RV) to induce injury to cultured monolayers of human umbilical vein endothelial cells (HEC) was investigated. Injury was assessed in vitro using assays of cell lysis and cell detachment.

The role of inflammatory cells and their proteases in extravascular fibrinolysis.

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Extravascular fibrin formation and dissolution is a pivotal event in numerous inflammatory and malignant diseases. In inflammatory cells such as monocytes/macrophages, neutrophil granulocytes appear to interact intimately with hemostasis and regulate the activity of the cascade systems of

Induction of proteinase 3-anti-neutrophil cytoplasmic autoantibodies by proteinase 3-homologous bacterial protease in mice.

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Proteinase 3 (PR3) is the principal target of antineutrophil cytoplasmic autoantibodies (ANCA) associated with granulomatosis with polyangiitis. The aim of this study was to investigate whether bacterial PR3-homologous protease can induce autoantibodies to PR3 and ANCA-associated pathology in mice.

Kinetics of thrombomodulin release and endothelial cell injury by neutrophil-derived proteases and oxygen radicals.

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Thrombomodulin is a transmembranous glycoprotein of endothelial cells. In vitro it is a marker of endothelial cell injury. In vivo the levels of serum thrombomodulin are regarded as a parameter of activity in vasculitides. The latter are pathophysiologically determined by neutrophil-derived

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

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OBJECTIVE 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. RESULTS Drug-induced and

Vasculitis: an approach for physicians.

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In the absence of a satisfactory classification, a sequential approach to the problems of vasculitis is recommended to the clinician. Clinical recognition will result from a presentation of: i. a well-defined syndrome; ii. a visually identifiable vasculitis (cutaneous or retina);

Association of autoantibodies to myeloperoxidase with different forms of vasculitis.

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Antineutrophil cytoplasmic autoantibodies with specificity for myeloperoxidase (MPO) were found in 53 patient sera that were routinely submitted for antineutrophil cytoplasmic antibody determination. Based on clinical and histologic criteria, 15 of these 53 patients were classified as having

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