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Titolo:
Accelerated nephrotoxic nephritis is exacerbated in C1q-deficient mice
Autore:
Robson, MG; Cook, HT; Botto, M; Taylor, PR; Busso, N; Salvi, R; Pusey, CD; Walport, MJ; Davies, KA;
Indirizzi:
Univ London Imperial Coll Sci Technol & Med, Hammersmith Hosp, Div Med, Rheumatol Sect,Sch Sci Technol & Med, London W12 0NN, England Univ London Imperial Coll Sci Technol & Med London England W12 0NN gland Univ London Imperial Coll Sci Technol & Med, Hammersmith Hosp, Dept Histopathol, Sch Sci Technol & Med, London W12 0NN, England Univ London Imperial Coll Sci Technol & Med London England W12 0NN gland CHU Vaudois, Lab Rhumatol, CH-1011 Lausanne, Switzerland CHU Vaudois Lausanne Switzerland CH-1011 , CH-1011 Lausanne, Switzerland
Titolo Testata:
JOURNAL OF IMMUNOLOGY
fascicolo: 11, volume: 166, anno: 2001,
pagine: 6820 - 6828
SICI:
0022-1767(20010601)166:11<6820:ANNIEI>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
EXPERIMENTAL MEMBRANOUS NEPHROPATHY; SYSTEMIC LUPUS-ERYTHEMATOSUS; TERMINAL COMPLEMENT PATHWAY; PROCOAGULANT ACTIVITY; APOPTOTIC CELLS; DEFICIENT MICE; EXPERIMENTAL GLOMERULONEPHRITIS; CRESCENTIC GLOMERULONEPHRITIS; INFLAMMATORY RESPONSES; PLASMINOGEN ACTIVATORS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Davies, KA Univ London Imperial Coll Sci Technol & Med, Hammersmith Hosp, Div Med, Rheumatol Sect,Sch Sci Technol & Med, Du Cane Rd, London W12 0NN, England Univ London Imperial Coll Sci Technol & Med Du Cane Rd London England W12 0NN
Citazione:
M.G. Robson et al., "Accelerated nephrotoxic nephritis is exacerbated in C1q-deficient mice", J IMMUNOL, 166(11), 2001, pp. 6820-6828

Abstract

C1q deficiency strongly predisposes to the development of systemic lupus erythematosus in humans and mice. We used the model of accelerated nephrotoxic nephritis in C1q-deficient mice to explore the mechanisms behind these associations. C1q-deficient mice developed severe glomerular thrombosis within 4 days of induction of disease, whereas wild-type mice developed mild injury. These findings suggest that C1q protects from immune-mediated glomerular injury. This exacerbated thrombosis was also seen in mice triply deficient in C1q, factor B, and C2, excluding a major pathogenic role for the alternative pathway of complement in this phenomenon. However, these mice did not develop elevated creatinine levels. No exacerbation of accelerated nephrotoxic nephritis was observed in mice doubly deficient in factor B and C2,suggesting a protective role for C1q against renal inflammation that is proximal to C2 activation. There were increased murine IgG deposits, neutrophil numbers, and apoptotic cells in the glomeruli of C1q-deficient mice compared with wild-type mice. Renal expression of genes encoding procoagulant proteins was also enhanced in C1q-deficient mice. The increased IgG depositsand apoptotic cells in the glomeruli of C1q-deficient mice suggest that the exacerbation of disease may be due to a defect in the clearance of immunecomplexes and/or apoptotic cells from their kidneys.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/12/20 alle ore 19:39:52