Mechanisms of Disease: pathogenesis and treatment of ANCA-associated vasculitides. (Q36667809)

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22 December 2019

review article

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title

Mechanisms of Disease: pathogenesis and treatment of ANCA-associated vasculitides (English)

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22 December 2019

2

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22 December 2019

1

Cees G M Kallenberg

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22 December 2019

author name string

Coen A Stegeman

series ordinal

3

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22 December 2019

publication date

1 December 2006

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Nature Clinical Practice Rheumatology

22 December 2019

published in

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22 December 2019

volume

2

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22 December 2019

page(s)

661-670

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22 December 2019

issue

12

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The American College of Rheumatology 1990 criteria for the classification of vasculitis. Introduction

22 December 2019

cites work

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Medium- and large-vessel vasculitis

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Small-vessel vasculitis

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Immune complex deposits in ANCA-associated crescentic glomerulonephritis: a study of 126 cases

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Anti-neutrophil cytoplasmic antibodies: current diagnostic and pathophysiological potential

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The role of antineutrophil cytoplasmic antibody (c-ANCA) testing in the diagnosis of Wegener granulomatosis. A literature review and meta-analysis

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Diagnostic value of standardized assays for anti-neutrophil cytoplasmic antibodies in idiopathic systemic vasculitis. EC/BCR Project for ANCA Assay Standardization

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Prevalence and clinical significance of antineutrophil cytoplasmic antibodies in Churg-Strauss syndrome

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Antineutrophil cytoplasmic antibodies and the Churg-Strauss syndrome

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Churg-Strauss syndrome: just one disease entity?

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Antiproteinase 3- and antimyeloperoxidase-associated vasculitis

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Prediction of relapses in Wegener's granulomatosis by measurement of antineutrophil cytoplasmic antibody levels: a prospective study

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Anti-neutrophil cytoplasmic antibody (ANCA) levels directed against proteinase-3 and myeloperoxidase are helpful in predicting disease relapse in ANCA-associated small-vessel vasculitis

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Anti-neutrophil cytoplasmic autoantibodies induce neutrophils to degranulate and produce oxygen radicals in vitro

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Neutrophil activation by anti-proteinase 3 antibodies in Wegener's granulomatosis: role of exogenous arachidonic acid and leukotriene B4 generation

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Neutrophil-activating potential of antineutrophil cytoplasm autoantibodies

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Activation of granulocytes by anti-neutrophil cytoplasmic antibodies (ANCA): a Fc gamma RII-dependent process

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Activation of the G(i) heterotrimeric G protein by ANCA IgG F(ab')2 fragments is necessary but not sufficient to stimulate the recruitment of those downstream mediators used by intact ANCA IgG.

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7 January 2021

Membrane expression of proteinase 3 is genetically determined

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Neutrophil membrane expression of proteinase 3 (PR3) is related to relapse in PR3-ANCA-associated vasculitis

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7 January 2021

Constitutive membrane expression of proteinase 3 (PR3) and neutrophil activation by anti-PR3 antibodies

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7 January 2021

Expression of myeloperoxidase (MPO) by neutrophils is necessary for their activation by anti-neutrophil cytoplasm autoantibodies (ANCA) against MPO

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7 January 2021

Antineutrophil cytoplasmic antibodies induce human monocytes to produce oxygen radicals in vitro

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7 January 2021

Antineutrophil cytoplasmic antibodies induce decreased CD62L expression and enhanced metabolic activity in monocytes

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7 January 2021

Association of chronic nasal carriage of Staphylococcus aureus and higher relapse rates in Wegener granulomatosis

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7 January 2021

Trimethoprim-sulfamethoxazole (co-trimoxazole) for the prevention of relapses of Wegener's granulomatosis. Dutch Co-Trimoxazole Wegener Study Group

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Antineutrophil cytoplasmic antibodies stabilize adhesion and promote migration of flowing neutrophils on endothelial cells

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Anti-proteinase-3 (PR3) antibodies (C-ANCA) recognize various targets on the human umbilical vein endothelial cell (HUVEC) membrane

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7 January 2021

Endothelial cells and renal epithelial cells do not express the Wegener's autoantigen, proteinase 3.

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7 January 2021

Off balance: T-cells in antineutrophil cytoplasmic antibody (ANCA)-associated vasculitides

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7 January 2021

Antimyeloperoxidase-associated proliferative glomerulonephritis: an animal model

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Antimyeloperoxidase-associated lung disease. An experimental model

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Antineutrophil cytoplasmic autoantibodies specific for myeloperoxidase cause glomerulonephritis and vasculitis in mice

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7 January 2021

Aggravation of anti-myeloperoxidase antibody-induced glomerulonephritis by bacterial lipopolysaccharide: role of tumor necrosis factor-alpha

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7 January 2021

Antineutrophil cytoplasm antibodies directed against myeloperoxidase augment leukocyte-microvascular interactions in vivo

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7 January 2021

The role of neutrophils in the induction of glomerulonephritis by anti-myeloperoxidase antibodies

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7 January 2021

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7 January 2021

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7 January 2021

Identifiers

DOI

10.1038/NCPRHEUM0355

1 reference

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:17133251%20AND%20SRC:MED&resulttype=core&format=json

22 December 2019

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