Abstract
Neural stem cells (NSCs) are shielded from viral infection by interferon (IFN) defense. As individuals age, activation of NSC decreases with a significant decline of stemness marker Sex-determining region Y box 2 (Sox2) while IFN signaling enhances (Kalamakis etal, 2019). Given that low-level type-I IFN under normal physiological conditions can promote dormant hematopoietic stem cell differentiation (Baldridge etal, 2010), whether there is an inner connection between IFN signaling and NSC function remains elusive. In this issue of EMBO Molecular Medicine, Carvajal Ibanez etal (2023) reveal that IFN-β, a type-I interferon, induces cell-type-specific interferon-stimulated genes (ISGs) and regulates global protein synthesis by orchestrating mTOR1 activity and stem cell cycle that retain NSCs at the G0 phase and repress Sox2 expression. As a consequence, NSCs exit the activation state and become inclined to differentiation.
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