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HIF1α is required for NK cell metabolic adaptation during virus infection

by Yang, Li-Ping , Yokoyama, Wayne M , Yao, Cong-Hui , Bigley, Tarin M , Park, Eugene , Davidson, Rebecca M , Piersma, Sytse J , Victorino, Francisco , Benoit, Jeanne , Patti, Gary J , Lauron, Elvin J

in Adaptation / Animals / Apoptosis / BIM protein / Caspase / Cell growth / Cell Proliferation / Cytokines / Cytomegalovirus / Cytomegalovirus Infections - virology / Experiments / Glucose / Glucose metabolism / HIF1α / Hypoxia / Hypoxia-Inducible Factor 1, alpha Subunit - genetics / Hypoxia-Inducible Factor 1, alpha Subunit - metabolism / Hypoxia-inducible factors / Immunology and Inflammation / Infections / Inflammation / Killer Cells, Natural - immunology / Lymphocyte Activation / MCMV / Metabolism / Mice / Morbidity / Muromegalovirus - physiology / Natural killer cells / NK cells / Pathogens / Protein expression / Protein turnover / Proteins / Viruses

2021

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HIF1α is required for NK cell metabolic adaptation during virus infection

2021

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2021

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Journal Article

HIF1α is required for NK cell metabolic adaptation during virus infection

Yang, Li-Ping,

Yokoyama, Wayne M,

Yao, Cong-Hui,

Bigley, Tarin M,

Park, Eugene,

Davidson, Rebecca M,

Piersma, Sytse J,

Victorino, Francisco,

Benoit, Jeanne,

Patti, Gary J,

Lauron, Elvin J

2021

Overview

Natural killer (NK) cells are essential for early protection against virus infection and must metabolically adapt to the energy demands of activation. Here, we found upregulation of the metabolic adaptor hypoxia-inducible factor-1α (HIF1α) is a feature of mouse NK cells during murine cytomegalovirus (MCMV) infection in vivo. HIF1α-deficient NK cells failed to control viral load, causing increased morbidity. No defects were found in effector functions of HIF1αKO NK cells; however, their numbers were significantly reduced. Loss of HIF1α did not affect NK cell proliferation during in vivo infection and in vitro cytokine stimulation. Instead, we found that HIF1α-deficient NK cells showed increased expression of the pro-apoptotic protein Bim and glucose metabolism was impaired during cytokine stimulation in vitro. Similarly, during MCMV infection HIF1α-deficient NK cells upregulated Bim and had increased caspase activity. Thus, NK cells require HIF1α-dependent metabolic functions to repress Bim expression and sustain cell numbers for an optimal virus response.

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Publisher

eLife Sciences Publications Ltd,eLife Sciences Publications, Ltd

Subject

/ Animals

/ Caspase