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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.

Type

Journal article

Journal

Blood

Publication Date

05/2012

Volume

119

Pages

4527 - 4531

Addresses

Inserm U1065, Centre Méditerranéen de Médecine Moléculaire, Nice, France.

Keywords

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