Promotion of lupus in NZB x NZWF1 mice by plasmids encoding interferon (IFN)-gamma but not by those encoding interleukin (IL)-4.
The present study extended our previous observation that interferon (IFN)-gamma may be responsible for the active disease that develops in NZB x NZWF1 mice and serves as a model for human systemic lupus erythematosus. Treatments with cytokine-encoding plasmids were delivered intraperitoneally every 4 weeks, starting at 3 months of age (i.e. before the onset of lupus). In comparison with the control plasmid and the IL-4-encoding plasmid, the IFN-gamma-encoding plasmid promoted increased blood urea nitrogen values and reduced the survival rate, and these changes were accompanied by the development of anti-nuclear antibody. There were no differences, however, between treatment with control plasmids and treatment with IL-4-encoding plasmids in terms of the development of lupus. The findings clearly indicated that IFN-gamma but not IL-4 contributed to the development of lupus in the NZB x NZWF1 mice.
D000818:Animals; D000974:Antibodies, Antinuclear / Q000097:blood; D001806:Blood Urea Nitrogen; D004195:Disease Models, Animal; D005260:Female; D007371:Interferon-gamma / Q000235:genetics / Q000276:immunology*; D015847:Interleukin-4 / Q000235:genetics / Q000276:immunology*; D008180:Lupus Erythematosus, Systemic / Q000097:blood / Q000235:genetics / Q000276:immunology* / Q000401:mortality; D051379:Mice; D008814:Mice, Inbred NZB; D010957:Plasmids; D015996:Survival Rate
D000974:Antibodies, Antinuclear; D015847:Interleukin-4; D007371:Interferon-gamma