Histone deacetylase 3 couples mitochondria to drive inflammation by configuring fatty acid oxidation

Immune cell function is crucially dependent on specific metabolic programs dictated by mitochondria, including the oxidation of nutrients, synthesis of macromolecules, and post-translational modifications. Mitochondrial adaptations have been intimately linked to acute and chronic inflammation, but the metabolic cues and precise mechanisms remain unclear. Here we reveal an essential role of macrophage expression of histone deacetylase 3 (HDAC3) in shaping mitochondrial adaptations for IL-1β production through non-histone deacetylation. Unprocessed westernblot data was uploaded in this dataset.