Abstract
Macroautophagy/autophagy and inflammation are 2 intertwined processes vital for immune cells to perform their functions. Under resting conditions, autophagy acts as a brake to suppress inflammation in microglia. Upon signal stimulation, their fine-tuned interplay is pivotal for proper response to stress. How inflammatory signals remove this autophagy brake on inflammation remains unclear. In a recent study, we showed that the stress kinase MAPK14/p38α in microglia senses the inflammatory cue lipopolysaccharide (LPS), directly phosphorylates and inhibits ULK1, relieves the autophagic inhibition on the inflammatory machinery, and thus allows for a full immune response.