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*Substance via MeSH
Medline Plus Health Information
*Lupus
The Journal of Immunology, 2005, 174: 2499-2506.
Copyright © 2005 by The American Association of Immunologists

IFN-{alpha} Induces Early Lethal Lupus in Preautoimmune (New Zealand Black x New Zealand White)F1 but Not in BALB/c Mice1

Alexis Mathian*, Arthur Weinberg{dagger}, Mike Gallegos*, Jacques Banchereau2,3,* and Sophie Koutouzov2,4,*

* Baylor Institute for Immunology Research, Dallas, TX 75204; and {dagger} Department of Pathology, Children’s Hospital, Dallas, TX 75235

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))F1, 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, ~9 and ~18 wk, at a time when all untreated (NZB x NZW)F1 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)F1 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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