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Titolo:
Cutting edge: C1q protects against the development of glomerulonephritis independently of C3 activation
Autore:
Mitchell, DA; Taylor, PR; Cook, HT; Moss, J; Bygrave, AE; Walport, MJ; Botto, M;
Indirizzi:
Imperial Coll Sch Med, Rheumatol Sect, London, England Imperial Coll Sch Med London England d, Rheumatol Sect, London, England Imperial Coll Sch Med, Dept Histopathol, London, England Imperial Coll SchMed London England Dept Histopathol, London, England
Titolo Testata:
JOURNAL OF IMMUNOLOGY
fascicolo: 10, volume: 162, anno: 1999,
pagine: 5676 - 5679
SICI:
0022-1767(19990515)162:10<5676:CECPAT>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
GENE-EXPRESSION; ARTHUS REACTION; INFLAMMATORY RESPONSES; COMPLEMENT DEFICIENCY; FC-RECEPTORS; CELLS; MICE; ERYTHEMATOSUS; KERATINOCYTES; AUTOANTIBODY;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
23
Recensione:
Indirizzi per estratti:
Indirizzo: Botto, M Hammersmiththosp, Imperial Coll Sch Med, Div Med, Rheumatol Sect,Hammersmi Hammersmith Hosp Hammersmith Campus,Du Cane Rd London England W12 0NN
Citazione:
D.A. Mitchell et al., "Cutting edge: C1q protects against the development of glomerulonephritis independently of C3 activation", J IMMUNOL, 162(10), 1999, pp. 5676-5679

Abstract

C1q-deficient (C1qa(-/-)) mice develop antinuclear Abs and glomerulonephritis (GN) characterized by multiple apoptotic bodies. To explore the contribution of C3 activation to the induction of spontaneous GN, C1qa(-/-) mice were crossed with factor B- and C2-deficient (H2-Bf/C2(-/-)) mice. GN was present in 64% of the 45 C1qa/H2-Bf/C2(-/-) mice compared with 8% of the 65 H2-Bf/ C2(-/-) mice and none of the 24 wild-type controls. IgG was detected in the glomeruli of diseased C1qa/H2-Bf/C2(-/-) kidneys. However, glomerular staining for C3 was absent, Increased numbers of glomerular apoptotic bodies were detected in undiseased C1qa/H2-Bf/C2(-/-) kidneys. These findings support the hypothesis that Clq may play a role in the clearance of apoptotic cells without the necessity for C3 activation and demonstrate that the activation of C3 is not essential for the development of GN in this spontaneous model of lupus-like disease.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/12/20 alle ore 19:42:53