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Titolo:
INDUCTION OF AUTOIMMUNE MYOCARDITIS IN INTERLEUKIN-2-DEFICIENT MICE
Autore:
GRASSL G; PUMMERER CL; HORAK I; NEU N;
Indirizzi:
INNSBRUCK UNIV,KLIN KINDERHEILKUNDE,DEPT PEDIAT,ANICHSTR 35 A-6020 INNSBRUCK AUSTRIA INNSBRUCK UNIV,KLIN KINDERHEILKUNDE,DEPT PEDIAT A-6020 INNSBRUCK AUSTRIA UNIV WURZBURG,INST VIROL & IMMUNOBIOL D-8700 WURZBURG GERMANY
Titolo Testata:
Circulation
fascicolo: 7, volume: 95, anno: 1997,
pagine: 1773 - 1776
SICI:
0009-7322(1997)95:7<1773:IOAMII>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
B3 MYOCARDITIS; DISEASE; CYCLOSPORINE; EXPRESSION; MECHANISMS; RECEPTOR; GENE;
Keywords:
MYOCARDITIS; IMMUNOLOGY; MYOSIN; INTERLEUKINS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
19
Recensione:
Indirizzi per estratti:
Citazione:
G. Grassl et al., "INDUCTION OF AUTOIMMUNE MYOCARDITIS IN INTERLEUKIN-2-DEFICIENT MICE", Circulation, 95(7), 1997, pp. 1773-1776

Abstract

Background Interleukin (IL)-2 is an important growth and survival factor for T cells and plays a crucial role in inflammation. Myosin-induced myocarditis is strictly dependent on activated T cells and is a model for postinfectious inflammatory heart disease in humans. To explorethe role of IL-2 in myocarditis, we injected mice genetically deficient for IL-2 with cardiac myosin. Because it is conceivable that the lack of IL-2 either promotes or ameliorates the disease, we selected mouse strains that differ in their susceptibility to cardiac myosin-induced myocarditis. Methods and Results Mice from a susceptible strain (C3H) that were rendered IL-2 deficient by gene targeting (IL-2(-/-) mice) and littermate controls were immunized twice with purified cardiac myosin at a 7-day interval. Three weeks after the first immunization, hearts were obtained for histopathological and immunohistochemical analysis. Sera were tested for autoantibodies to the cardiac myosin isoform by enzyme-linked immunosorbent assay. The majority of C3H IL-2(-/-) mice developed severe myocarditis accompanied by high-titer myosin autoantibodies. In C57BL/6 mice, which develop only little myocarditis onmyosin immunization, lack of IL-2 did not increase susceptibility to the disease. Moreover, the composition of the inflammatory infiltrate in C3H IL-2(-/-) mice was virtually identical to that seen in the wild-type strain. Conclusions Our data provide the first genetic evidence that in cardiac myosin-immunized mice, IL-2 has no essential role for the development of autoimmune heart disease and the generation of myosin autoantibodies.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/11/20 alle ore 15:45:47