BCL-6: a possible missing link for anti-inflammatory PPAR-δ signalling in pancreatic beta cells

Aims/hypothesis Inflammatory mediators contribute to pancreatic beta cell death in type 1 diabetes. Beta cells respond to cytokine exposure by activating gene networks that alter cellular metabolism, induce chemokine release (thereby increasing insulitis), and cause apoptosis. We have previously shown by microarray analysis that exposure of INS-1E cells to IL-1β + IFN-γ induces the transcription factor peroxisome proliferator-activated receptor (Ppar)-δ and several of its target genes. PPAR-δ controls cellular lipid metabolism and is a major regulator of inflammatory responses. We therefore examined the role of PPAR-δ in cytokine-treated beta cells.