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Titolo:
Anti-proteinase 3 antibody activation of neutrophils can be inhibited by alpha 1-antitrypsin
Autore:
Rooney, CP; Taggart, C; Coakley, R; McElvaney, NG; ONeill, SJ;
Indirizzi:
Beaumont Hosp, Royal Coll Surg Ireland, Educ & Res Ctr, Dept Med,Div Resp Res, Dublin 2, Ireland Beaumont Hosp Dublin Ireland 2 Dept Med,Div Resp Res, Dublin 2, Ireland
Titolo Testata:
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
fascicolo: 6, volume: 24, anno: 2001,
pagine: 747 - 754
SICI:
1044-1549(200106)24:6<747:A3AAON>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
HUMAN POLYMORPHONUCLEAR LEUKOCYTES; WEGENERS GRANULOMATOSIS; SYSTEMIC VASCULITIS; ENDOTHELIAL-CELLS; IN-VITRO; AUTOANTIBODIES; ALPHA(1)-ANTITRYPSIN; MYELOPEROXIDASE; RELEVANCE; ELASTASE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
31
Recensione:
Indirizzi per estratti:
Indirizzo: O'Neill, SJ Beaumont Hosp, Royal Coll Surg Ireland, Educ & Res Ctr, Dept Med,Div Resp Res, Beaumont Rd, Dublin 2, Ireland Beaumont Hosp Beaumont Rd Dublin Ireland 2 Dublin 2, Ireland
Citazione:
C.P. Rooney et al., "Anti-proteinase 3 antibody activation of neutrophils can be inhibited by alpha 1-antitrypsin", AM J RESP C, 24(6), 2001, pp. 747-754

Abstract

Wegener's granulomatosis (WG) is classically associated with the presence of cytoplasmic antineutrophil cytoplasmic autoantibodies (c-ANCA), Proteinase 3 (PR3), the target antigen for c-ANCA, is inhibited by the antiproteasealpha1-antitrypsin (A1AT), and recent studies have demonstrated that WG patients who are A1AT-deficient have a worse clinical course, suggesting thata protease-antiprotease imbalance may play a role in WG. We evaluated the effect of A1AT on anti-PR3 antibody-induced activation of neutrophils. The neutrophil was chosen because of its central role in the pathogenesis of WG. Isolated neutrophils from healthy controls were incubated with tumor necrosis factor (TNF)-alpha to induce surface expression of PR3, Subsequently, they were stimulated with a monoclonal antibody to PR3, resulting in a significant increase in respiratory burst. Addition of A1AT (1 mg/ml) to the TNF-alpha -primed cells before the addition of the anti-PR3 antibody resultedin a 47% reduction in anti-PR3 antibody-induced activation. A1AT mediated this inhibitory action by preventing anti-PR3 antibody binding to PR3 on the cell, thereby preventing the PR3-Fc gamma R11a cross-linkage required forcell activation. Further, anti-PR3 antibody-induced activation of neutrophils from WG patients can be reduced by 56% with A1AT. These data suggest that protease-antiprotease interactions may play a pivotal role in neutrophilactivation in WG.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 03/07/20 alle ore 01:51:10