Differential actions of IL-I alpha and IL-I beta in glial cells share common IL-I signalling pathways

The cytokine interleukin (IL)-I plays important roles in peripheral and central inflammation via the actions of two ligands IL-Ialpha and IL-Ibeta that bind to the IL-I type I receptor (IL-I RI) and trigger identical responses. However, some recent evidence suggests that IL-Ialpha and IL-Ibeta may have differential actions in the CNS. The aim of this study was to characterise the molecular mechanisms responsible for their differential actions in the brain. We show that, while IL-Ialpha and IL-Ibeta induce identical IL-I signalling pathways, IL-Ibeta is significantly more potent than IL-Ialpha in stimulating IL-6 release in primary mixed glia. These data suggest that the differential effects of IL-Ialpha and IL-Ibeta on glial cells are mediated by alternative pathways to the classical IL-I signalling cascade. NeuroReport 16:153-157 (C) 2005 Lippincott Williams Wilkins.