Antibodies to Neutrophil Cytoplasmic Antigen in Systemic Vasculitis

Venning, M. C.; Arfeen, Shahab; Bird, AngusGraham

doi:10.1016/s0140-6736(87)91030-0

Cited by 54 publications

(20 citation statements)

References 3 publications

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“…The vascular lesions form a continuum from renal-limited necrotizing and crescentic glomerulonephritis to systemic vasculitis (1,(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15). ANCA react with constituents of neutrophil primary granules and monocyte lysosomes (1,6,(16)(17)(18).…”

mentioning

confidence: 99%

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

Falk

Terrell

Charles

et al. 1990

Proc. Natl. Acad. Sci. U.S.A.

1,161

730

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Anti-neutrophil cytoplasmic autoantibodies (ANCA) are in the circulation of most patients with pauciimmune necrotizing vasculitis and pauci-immune crescentic glomerulonephritis. The current study demonstrates an effect of these autoantibodies on neutrophil function in vitro. ANCA cause normal human neutrophils to undergo an oxidative burst and degranulate. Both ANCA phenotypes (i.e., cytoplasmicpattern ANCA and myeloperoxidase-specific ANCA) induce neutrophil activation. ANCA sera and purified immunoglobulins significantly increase the release ofreactive oxygen species when compared with controls. ANCA, in a dose-dependent manner, induce the release of primary granule contents. These effects are markedly enhanced by priming neutrophils with tumor necrosis factor. Flow cytometry studies demonstrate the presence of myeloperoxidase on the surface of neutrophils after cytokine priming, indicating that primed neutrophils have ANCA antigens at their surfaces to interact with ANCA. These observations suggest an in vivo pathogenetic role for ANCA. We propose that, in patients with necrotizing vasculitis, ANCA-induced release of toxic oxygen radicals and noxious granule enzymes from cytokine-primed neutrophils could be mediating vascular inflammation.

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mentioning

confidence: 99%

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

Falk

Terrell

Charles

et al. 1990

Proc. Natl. Acad. Sci. U.S.A.

1,161

730

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“…Sub sequently, a number of investigators, using a variety of detection assays, confirmed that IgG ANCA was a sensi tive and specific marker for WG [6,7]. In early studies, the only other condition in which IgG ANCA was found with substantial frequency was microscopic polyarteritis [8,20]. However, the pathologic distinction between microscopic polyarteritis and WG is not clear, and they may represent different ends of the spectrum of the same disease [21].…”

Section: Discussionmentioning

confidence: 99%

IgA Antineutrophil Cytoplasmic Antibody in Henoch-Schönlein Purpura

Saulsbury

Kirkpatrick²,

Bolton

1991

Am J Nephrol

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Sera from 29 children with acute Henoch-Schönlein purpura were tested for IgA antineutrophil cytoplasmic antibody (ANCA) and for IgA rheumatoid factor (RF). All sera were negative for IgA ANCA by indirect immunofluorescence, but 13 of 29 patients had weakly positive results for IgA ANCA when tested using an enzyme immunoassay. Sixteen of 29 children were IgA RF seropositive. IgA RF seropositive patients had significantly higher titers of IgA ANCA as compared with IgA RF seronegative patients (p = 0.0002). Indeed, of the 16 patients who were IgA RF seropositive, 13 also had positive tests for IgA ANCA, while none of the IgA RF seronegative patients had positive tests for IgA ANCA (p = 0.00001). Removal of IgA RF from eight sera by adsorption with immobilized IgG produced comparable reductions in the titers of both IgA RF and IgA ANCA. We conclude that IgA ANCA is not an important serologic marker in Henoch-Schönlein purpura, but the presence of serum IgA RF may produce weak false-positive results for IgA ANCA in some patients.

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“…To reduce the adverse effects of treatment the dose of oral prednisolone was reduced rapidly to [10][11][12][13][14][15] mg/day once the patient was clearly responding. The dose of oral cyclophosphamide was maintained for at least one year and gradually reduced while the patient was monitored closely for evidence of relapse.…”

Section: Treatmentmentioning

confidence: 99%

“…Ear-Fifteen patients had disease of the ear, the commonest presenting features being conductive deafness (13) and pain (11). Eight had a discharge, often purulent, six had serous otitis media, and three had otitis externa.…”

Section: Introductionmentioning

confidence: 99%

Ear, nose, and throat symptoms in subacute Wegener's granulomatosis.

1989

BMJ

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Antibodies to Neutrophil Cytoplasmic Antigen in Systemic Vasculitis

Cited by 54 publications

References 3 publications

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

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

IgA Antineutrophil Cytoplasmic Antibody in Henoch-Schönlein Purpura

Ear, nose, and throat symptoms in subacute Wegener's granulomatosis.

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Antibodies to Neutrophil Cytoplasmic Antigen in Systemic Vasculitis

Cited by 54 publications

References 3 publications

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

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

IgA Antineutrophil Cytoplasmic Antibody in Henoch-Sch&ouml;nlein Purpura

Ear, nose, and throat symptoms in subacute Wegener's granulomatosis.

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IgA Antineutrophil Cytoplasmic Antibody in Henoch-Schönlein Purpura