In diabetes, pancreatic islets are subjected to high levels of inflammatory mediators that can lead to beta cell destruction. We recently showed that pancreatic islet cells derived from MIF-deficient (MIF-KO) mice are resistant to apoptosis induction by the cytotoxic stimuli of cytokines. Here we show that MIF-KO islets under cytokine (IFN-γ+TNF- α+IL-1β) stimulation express and secrete significantly lower amounts of IL-1β, while the expression of caspase-1 mRNA is not influenced by MIF deficiency. These data suggest that MIF-KO islets possess an innate defect in the process of IL-1 β synthesis and secretion.