IL-18 cDNA vaccination protect mice from spontaneous lupus-like disease (Articolo in rivista)

Type
Label
  • IL-18 cDNA vaccination protect mice from spontaneous lupus-like disease (Articolo in rivista) (literal)
Anno
  • 2003-01-01T00:00:00+01:00 (literal)
Alternative label
  • Bossù P., Neumann D., Del Giudice E., Ciaramella A., Gloaguen I., Fantuzzi G., Dinarello C.A., Di Carlo E., Musiani P., Meroni P.L., Caselli G., Ruggiero P, Boraschi D. (2003)
    IL-18 cDNA vaccination protect mice from spontaneous lupus-like disease
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Bossù P., Neumann D., Del Giudice E., Ciaramella A., Gloaguen I., Fantuzzi G., Dinarello C.A., Di Carlo E., Musiani P., Meroni P.L., Caselli G., Ruggiero P, Boraschi D. (literal)
Pagina inizio
  • 14181 (literal)
Pagina fine
  • 14186 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 100 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#descrizioneSinteticaDelProdotto
  • La pubblicazione dimostra che la citochina IL-18 ha un ruolo central nella patogenesi delle malattie autoimmuni e che con un approccio di vaccinazione terapeutica anti-IL-18 endogena è possibile ottenere un miglioramento significativo della malattia autoimmune, incluso l'aumento della sopravvivenza. Nuova prospettiva terapeutica. (literal)
Note
  • ISI Web of Science (WOS) (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • PB: Università di Roma Tor Vergata, Roma DN: Dept. Pharmacology, Hannover Medical School, Germania EDG, AC, GC: centro Ricerche Dompé SpA, L’Aquila IG: Consorzio Biolaq, L’Aquila GF, CAD: Dept. Medicine, University of Colorado Health Sciences Center, Denver, CO, USA EDC, PM: Dip. Oncologia e Neuroscienze, Università di Chieti PLM: Dip. Medicina Interna, Università di Milano, IRCCS IAI, Milano PR: Centro Ricerche, Chiron SpA, Siena DB: Istituto di Tecnologie Biomediche, CNR, Pisa (literal)
Titolo
  • IL-18 cDNA vaccination protect mice from spontaneous lupus-like disease (literal)
Abstract
  • The lupus-like autoimmune syndrome of MRL/Mp-Tnfrsf6lpr (lpr) mice is characterized by progressive lymphadenopathy and autoantibody production, leading to early death from renal failure. Activation of T helper lymphocytes is one of the events in the pathogenesis of the disease in these mice and likely in human systemic lupus erythematosus. Among T helper lymphocyte-dependent cytokines, IFN-gamma plays a pivotal role in the abnormal cell activation and in the fatal development of the lpr disease. IL 18, an inducer of IFN-gamma in T lymphocytes and natural killer cells, may contibute to the disease because cells from lpr mice are hyper-sensitive to IL-18 and express high levels of IL 18. To assess the contribution of IL-18 to the pathogenesis in the animal model, in vivo inhibition of IL-18 was attempted. Young lpr mice were vaccinated against autologous IL-18 by repeated administration of a cDNA coding for the murine IL 18 precursor. Vaccinated mice produced autoantibodies to murine IL-18 and exhibited a significant and IFN-gamma production as well as less glomerulonephritis and renal damage. Moreover, mortality was significantly delayed in anti-IL-18-vaccinated mice. These studies support the concept that IL-18 plays a major role in the pathogenesis of the autoimmune syndrome of lpr mice and that a reduction in IL-18 activity could be a therapeutic strategy in autoimmune diseases. (literal)
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