INSULIN-SECRETING BETA-CELLS POSSESS SPECIFIC RECEPTORS FOR INTERLEUKIN-1-BETA

The effect of the cytokine interleukin-1β on the insulin secretory responsiveness of single β-cells (HIT-T15) was investigated. In the short-term, IL-1β induced a dosage-dependent stimulation of insulin release. In contrast, in the long-term, IL-1β, inhibited both basal and secretagogue-stimulated insulin secretion. We also demonstrate the simultaneous presence of specific high and low affinity binding sites for IL-1β on β-cells. IL-1β, which has been implicated in the pathogenesis of insulin-dependent diabetes, may therefore mediate its opposing effects on β-cells through a specific plasma membrane receptor. © 1990.