Sleep is hypothesized to play a restorative role on immune system. In addition, disturbed sleep is thought to impair host defense mechanisms. Chronic sleep deprivation is a common occurrence in modern society and has been observed in a number of chronic inflammatory conditions, such as systemic lupus erythematosus (SLE). The (NZB/W)F₁ mice develop autoimmune disease which strongly resembles SLE in humans, exhibiting high titers of antinuclear antibodies associated with development of rapidly progressive and lethal glomerulonephritis. Based on this evidence, the present study examined the onset and progress of lupus in as yet healthy female mice submitted to sleep deprivation. Sleep deprivation was accomplished by two 96h periods in the multiple platform method, when mice were ten-week old, and they were observed until twenty-eight weeks of age. Blood samples were collected from the orbital plexus fortnightly, in order to evaluate serum antinuclear antibodies and anti-double-stranded DNA. Proteinuria, longevity, as well as body weight were also assessed. The results indicated that mice submitted to SD exhibited an earlier onset of the disease, reflected by increased number of antinuclear antibodies. However, no statistical difference was found in other parameters analyzed. According to these results, SD could be considered a risk factor for the onset but not for the evolution of the disease.