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Induces Early Lethal Lupus in Preautoimmune (New Zealand Black x New Zealand White)F1 but Not in BALB/c Mice1
* Baylor Institute for Immunology Research, Dallas, TX 75204; and
Department of Pathology, Children’s Hospital, Dallas, TX 75235
Recent studies indicate that IFN-
is involved in pathogenesis of systemic lupus erythematosus. However, direct proof that IFN- 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- 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- 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- 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- were dose dependent. (NZB x NZW)F1 infused with purified murine IFN- also showed acceleration of lupus. Thus, prolonged expression of IFN- in vivo induces early lethal lupus in susceptible animals.
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