The MRL/lpr model of SLE resembles human lupus in its various immunopathologic characteristics including the presence of high-level IgG and anti-DNA antibody production and multisystem organ involvement (nephritis, arthritis, and vasculitis). Our previous studies have shown that IL-1 overactivity in B cells plays a potentially important role in driving IgG and autoantibody production. However, the underlying mechanisms determining IL-1 overactivity are poorly understood. We studied IL-lβgene expression and transcriptional rates in B cells derived from old and young MRL/lpr, MRL/+ +, and non-autoimmune control mice using semi-quantitative RT-PCR and the nuclear run-on assay. RT-PCR demonstrated increased steady-state IL-lβgene expression in B cells derived from old MRL/lpr mice as compared to either young MRL/lpr or control mice. Furthermore, IL-lβgene expression in B cells was associated with the presence of the lpr mutation because heightened IL-1βmessage was observed in RNA obtained from MRL/lpr but not MRL/+ + B cells. IL-lβtranscriptional rates measured by the nuclear run-on assay were very similar in B cells from old and young MRL/lpr and control mice. These observations suggest that IL-1 overactivity in B cells obtained from old diseased MRL/lpr results from heightened IL-lβmessage, is associated with the presence of the lpr mutation, and is likely to reflect post-transciptional stabilization of IL-1βmRNA.