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Autophagy is the process by which superfluous or damaged macromolecules or organelles are degraded by the lysosome. Pharmacologic and genetic evidence indicates that autophagy plays pleiotropic functions in cellular homeostasis, development, survival, and differentiation. The differentiation of human blood monocytes into macrophages is a caspase-dependent process when triggered ex vivo by colony stimulating factor-1. We show here, using pharmacologic inhibitors, siRNA approaches, and Atg7-/- mice, that autophagy initiated by ULK1 is required for proper colony stimulating factor-1-driven differentiation of human and murine monocytes. We also unravel a role for autophagy in macrophage acquisition of phagocytic functions. Collectively, these findings highlight an unexpected and essential role of autophagy during monocyte differentiation and acquisition of macrophage functions.

Original publication




Journal article



Publication Date





4527 - 4531


Animals, Autophagy, Autophagy-Related Protein 7, Autophagy-Related Protein-1 Homolog, Cathepsin B, Cell Differentiation, Cells, Cultured, Gene Expression Regulation, Humans, Macrophage Colony-Stimulating Factor, Macrophages, Mice, Mice, Knockout, Microtubule-Associated Proteins, Monocytes, Phagocytosis, Protein-Serine-Threonine Kinases, RNA, Small Interfering