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IL-15 reprogramming compensates for NK cell mitochondrial dysfunction in HIV-1 infection
Elia Moreno-Cubero1, Aljawharah Alrubayyi1, Stefan Balint2
1Nuffield Department of Clinical Medicine and.
JCI Insight
|February 22, 2024
Summary
Chronic HIV-1 infection impairs natural killer (NK) cell metabolism, specifically reducing oxidative phosphorylation (OXPHOS). However, interleukin-15 (IL-15) priming can restore NK cell function in these patients.
Area of Science:
- Immunology
- Cellular Metabolism
- Virology
Background:
- Cellular metabolism dynamically regulates immune cell function, impacting NK cell responses.
- Persistent HIV-1 infection causes chronic immune activation, NK cell redistribution, and dysregulation.
- Adaptive NK cell subpopulations, like NKG2C+ cells, expand during chronic infection.
Purpose of the Study:
- To investigate the metabolic characteristics of NK cell subsets in HIV-1 infection.
- To understand the impact of HIV-1 on the bioenergetics of adaptive NK cells.
- To explore strategies for restoring NK cell function in HIV-1 infection.
Main Methods:
- Flow cytometry to analyze NK cell subsets.
- Metabolic assays to assess oxidative phosphorylation (OXPHOS) and mitochondrial function.
- Interleukin-15 (IL-15) pretreatment to evaluate NK cell responses.
Main Results:
- HIV-1 infection leads to uniformly reduced OXPHOS in NK cells, irrespective of adaptive phenotypes.
- Mitochondrial defects, including depolarization and increased fission, were observed in NK cells from HIV-1 infected individuals.
- IL-15 pretreatment enhanced mammalian target of rapamycin complex 1 (mTORC1) activity and improved NK cell functionality.
Conclusions:
- HIV-1 infection impairs NK cell metabolic plasticity through mitochondrial defects.
- IL-15 priming represents a potential therapeutic strategy to boost NK cell responses in HIV-1 infection.
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