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Titolo:
Lethal autoimmune myocarditis in interferon-gamma receptor-deficient mice - Enhanced disease severity by impaired inducible nitric oxide synthase induction
Autore:
Eriksson, U; Kurrer, MO; Bingisser, R; Eugster, HP; Saremaslani, P; Follath, F; Marsch, S; Widmer, U;
Indirizzi:
Univ Basel Hosp, Med ICU, CH-4031 Basel, Switzerland Univ Basel Hosp Basel Switzerland CH-4031 CU, CH-4031 Basel, Switzerland Univ Zurich Hosp, Dept Pathol, CH-8091 Zurich, Switzerland Univ Zurich Hosp Zurich Switzerland CH-8091 CH-8091 Zurich, Switzerland Univ Zurich Hosp, Dept Med, Div Clin Immunol, CH-8091 Zurich, Switzerland Univ Zurich Hosp Zurich Switzerland CH-8091 CH-8091 Zurich, Switzerland
Titolo Testata:
CIRCULATION
fascicolo: 1, volume: 103, anno: 2001,
pagine: 18 - 21
SICI:
0009-7322(20010102)103:1<18:LAMIIR>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
HEART-DISEASE;
Keywords:
interferons; mice; autoimmunity; myocarditis; myosin; nitric oxide synthase;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
10
Recensione:
Indirizzi per estratti:
Indirizzo: Eriksson, U Univ Basel Hosp, Med ICU, Petersgraben 5, CH-4031 Basel, Switzerland Univ Basel Hosp Petersgraben 5 Basel Switzerland CH-4031 land
Citazione:
U. Eriksson et al., "Lethal autoimmune myocarditis in interferon-gamma receptor-deficient mice - Enhanced disease severity by impaired inducible nitric oxide synthase induction", CIRCULATION, 103(1), 2001, pp. 18-21

Abstract

Background-Interferon-gamma (IFN-gamma) is an essential cytokine in the regulation of inflammatory responses in autoimmune diseases. Little is known about its role in inflammatory heart disease. Methods and Results-We showed that IFN-gamma receptor-deficient mice (IFN-gammaR(-/-)) on a BALB/c background immunized with a peptide derived from cardiac alpha -myosin heavy chain develop severe myocarditis with high mortality. Although myocarditis subsided in wild-type mice after 3 weeks, IFN-gammaR(-/-) mice showed persistent disease. The persistent inflammation was accompanied by vigorous in vitro CD4 T-cell responses and impaired induciblenitric oxide synthase expression, together with evidence of impaired nitric oxide production in IFN-gammaR(-/-) hearts. Treatment of wild-type mice with the nitric oxide synthetase inhibitor N-nitro-L-arginine-methyl-ester enhanced in vitro CD4 T-cell proliferation and prevented healing of myocarditis. Conclusions-Our data provide evidence that IFN-gamma protects mice fi om lethal autoimmune myocarditis by inducing the expression of inducible nitricoxide synthase followed by the downregulation of T-cell responses.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/01/21 alle ore 03:00:15