IFN-alpha induces early lethal lupus in preautoimmune (New Zealand Black x New Zealand White) F1 but not in BALB/c mice.
J Immunol
; 174(5): 2499-506, 2005 Mar 01.
Article
en En
| MEDLINE
| ID: mdl-15728455
Recent studies indicate that IFN-alpha is involved in pathogenesis of systemic lupus erythematosus. However, direct proof that IFN-alpha is not only necessary, but also sufficient to induce lupus pathogenicity is lacking. In this study, we show that in vivo adenovector-mediated delivery of murine IFN-alpha results in preautoimmune (New Zealand Black (NZB) x New Zealand White (NZW))F(1), but not in normal, mice, in a rapid and severe disease with all characteristics of systemic lupus erythematosus. Anti-dsDNA Abs appeared as soon as day 10 after initiation of IFN-alpha treatment. Proteinuria and death caused by glomerulonephritis occurred in all treated mice within, respectively, approximately 9 and approximately 18 wk, at a time when all untreated (NZB x NZW)F(1) did not show any sign of disease. IFN-alpha in vivo induced an overexpression of B lymphocyte stimulator in circulation at similar levels in both the preautoimmune and the normal mouse strains. All effects elicited by IFN-alpha were dose dependent. (NZB x NZW)F(1) infused with purified murine IFN-alpha also showed acceleration of lupus. Thus, prolonged expression of IFN-alpha in vivo induces early lethal lupus in susceptible animals.
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Bases de datos:
MEDLINE
Asunto principal:
Interferón-alfa
/
Cruzamientos Genéticos
/
Lupus Eritematoso Sistémico
Límite:
Animals
Idioma:
En
Revista:
J Immunol
Año:
2005
Tipo del documento:
Article
País de afiliación:
Estados Unidos