Reliance on Cox10 and oxidative metabolism for antigen-specific NK cell expansion.

ABSTRACT: Natural killer (NK) cell effector functions are dependent on metabolic regulation of cellular function; however, less is known about in vivo metabolic pathways required for NK cell antiviral function. Mice with an inducible NK-specific deletion of Cox10, which encodes a component of electron transport chain complex IV, were generated to investigate the role of oxidative phosphorylation in NK cells during murine cytomegalovirus (MCMV) infection. Ncr1-Cox10^Δ/Δ mice had normal numbers of NK cells but impaired expansion of antigen-specific Ly49H⁺ NK cells and impaired NK cell memory formation. Proliferation in vitro and homeostatic expansion were intact, indicating a specific metabolic requirement for antigen-driven proliferation. Cox10-deficient NK cells upregulated glyc

SUBMITTER: Mah-Som AY 

PROVIDER: S-EPMC8229496 | biostudies-literature | 2021 Jun

REPOSITORIES: biostudies-literature