Abstract 2463 BET bromodomain inhibitors selectively attenuate IL-1-induced transcription of NF-κB targets in pancreatic β-cells

Inflammatory signaling is a hallmark of type 1 diabetes (T1D). In the pancreas, immune cells secrete proinflammatory cytokines like IL-1, which drive the transcriptional activation of NF-κB and its target inflammatory genes in insulin-producing β-cells. When this β-cell response to inflammatory stimuli is exaggerated or elongated, loss of β-cell function and mass can lead to T1D. Members of the bromodomain and extraterminal domain (BET) protein family function as epigenetic ‘readers' of lysine acetylation on histones and other nuclear proteins.