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Titolo:
IL-12-dependent, IFN-gamma-independent experimental glomerulonephritis
Autore:
Le Hir, M; Ryffel, B; Schatzmann, U;
Indirizzi:
Univ Zurich Irchel, Inst Anat, CH-8057 Zurich, Switzerland Univ Zurich Irchel Zurich Switzerland CH-8057 H-8057 Zurich, Switzerland Univ Cape Town, Dept Immunol, ZA-7700 Rondebosch, South Africa Univ Cape Town Rondebosch South Africa ZA-7700 Rondebosch, South Africa
Titolo Testata:
KIDNEY & BLOOD PRESSURE RESEARCH
fascicolo: 1, volume: 24, anno: 2001,
pagine: 27 - 32
SICI:
1420-4096(2001)24:1<27:IIEG>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
CRESCENTIC GLOMERULONEPHRITIS; DEFICIENT MICE; INTERFERON-GAMMA; MURINE GLOMERULONEPHRITIS; IL-12-DEFICIENT MICE; CYTOKINE RESPONSES; TH1 RESPONSES; SUSCEPTIBILITY; INJURY; IL-12;
Keywords:
glomerulonephritis; interleukin 12; interferon gamma; delayed-type hypersensitivity; Th-1;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
28
Recensione:
Indirizzi per estratti:
Indirizzo: Le Hir, M Univ Zurich Irchel, Inst Anat, Winterthurerstr 190, CH-8057 Zurich, Switzerland Univ Zurich Irchel Winterthurerstr 190 Zurich Switzerland CH-8057
Citazione:
M. Le Hir et al., "IL-12-dependent, IFN-gamma-independent experimental glomerulonephritis", KIDNEY BL P, 24(1), 2001, pp. 27-32

Abstract

There is evidence that crescentic glomerulonephritis initiated in rodents by heterologous antibodies against the glomerular basement membrane (anti-GBM glomerulonephritis) depends on a Th1-type immune reaction. Interleukin 12 (IL-12) is crucial for the development of Th1 helper cells, and interferon gamma (IFN-gamma) is a major proinflammatory product of these cells, in order to test the role of the two cytokines in anti-GEM glomerulonephritis we used mice lacking either the p40 chain of IL-12 (IL-12-/-) or the IFN-gamma receptor (IFN-gammaR-/-). Glomerulonephritis was induced by injecting a rabbit anti-GEM serum in mice preimmunized against rabbit IgG. Glomerulonephritis was assessed on the basis of proteinuria, immunofluorescence findings and histology. IL-12-/- mice were completely protected against glomerulonephritis. In contrast, IFN-gammaR-/- mice were more severely affected than wild-type mice. Similarly, cutaneous delayed-type hypersensitivity, a typical Th1 response, was abolished in the IL-12-/-, mice but increased in the IFN-gammaR-/- mice. The data obtained in IL-12-/- mice support the view thatcrescentic glomerulonephritis in this model represents a Th1 response. Since IFN-gamma is not required, other products of Th1 cells are likely to mediate glomerulonephritis. Copyright (C) 2001 S. Karger AG, Basel.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 10/04/20 alle ore 16:07:42