ArticleJCI insight2024
IL-15 reprogramming compensates for NK cell mitochondrial dysfunction in HIV-1 infection.
Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 20 citations in OpenAlex.
- DRP1 depletion protects NK cells from hypoxia-induced dysfunction.Redox report : communications in free radical research · 2026Article
- Siglec-7 orchestrates mitochondrial dynamics and metabolic reprogramming to restrain human NK cell cytotoxic function.The Journal of biological chemistry · 2026Article
- Natural killer cells against viral infection: from basic biology to immunotherapy.Precision clinical medicine · 2026Review
- Short-Chain Fatty Acids at the Crossroads of Microbiota, Immunometabolism, and Inflammation.Biomedicines · 2026Review
- CD49a expression defines a metabolically robust, cytokine-biased liver NK cell subset in rhesus macaques during lentivirus infection.Immunology and cell biology · 2026Article
- A Conserved Natural Killer Cell Transcriptional Fingerprint in Rhesus Macaque Models of Acute Viral Infections.AIDS research and human retroviruses · 2026Article
- HIV tri-specific killer engagers directly enhance NK cell function and safely expand NK cells in vivo.Cell reports. Medicine · 2026Article
- Arntl deficiency impairs NK cell function by reducing responsiveness to IL-15 and suppressing activation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Expanded adaptive NKG2C+ NK cells exhibit potent ADCC and functional responses against HBV-infected hepatoma cell lines.Cytotherapy · 2026Article
- Engineering with EP2/EP4 knockout and IL-15 transpresentation renders stem cell-derived NK cells self-persistent and resistant to PGE2 inhibition.Frontiers in immunology · 2026Article
- Chronic HBV infection impairs the glucose metabolism and effector function of NK cells via HBsAg/IL-15/mTOR axis.Cell death & disease · 2025Article
- Factors associated with resistance of HIV-1 reservoir viruses to neutralization by autologous IgG antibodies.The Journal of clinical investigation · 2025Article
- Immuno-cell metabolic changes in HIV-1 infection.Infectious diseases & immunity · 2025Review
- Immune dysregulation of decidual NK cells mediated by GRIM19 downregulation contributes to the occurrence of recurrent pregnancy loss.Molecular and cellular biochemistry · 2025Article
- Longitudinal analysis of rhesus macaque metabolome during acute SIV infection reveals disruption in broad metabolite classes.Journal of virology · 2025Article
- Elephant in the room: natural killer cells don't forget HIV either.Current opinion in HIV and AIDS · 2025Review
- Review
- Alterations in mitochondrial morphology as a key driver of immunity and host defence.EMBO reports · 2021Review
- Metabolism of Natural Killer Cells and Other Innate Lymphoid Cells.Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
13 authors at 6 institutions in 1 country.
Funding
Abstract
Dynamic regulation of cellular metabolism is important for maintaining homeostasis and can directly influence immune cell function and differentiation, including NK cell responses. Persistent HIV-1 infection leads to a state of chronic immune activation, NK cell subset redistribution, and progressive NK cell dysregulation. In this study, we examined the metabolic processes that characterize NK cell subsets in HIV-1 infection, including adaptive NK cell subpopulations expressing the activating receptor NKG2C, which expand during chronic infection. These adaptive NK cells exhibit an enhanced metabolic profile in HIV-1- individuals infected with human cytomegalovirus (HCMV). However, the bioenergetic advantage of adaptive CD57+NKG2C+ NK cells is diminished during chronic HIV-1 infection, where NK cells uniformly display reduced oxidative phosphorylation (OXPHOS). Defective OXPHOS was accompanied by increased mitochondrial depolarization, structural alterations, and increased DRP-1 levels promoting fission, suggesting that mitochondrial defects are restricting the metabolic plasticity of NK cell subsets in HIV-1 infection. The metabolic requirement for the NK cell response to receptor stimulation was alleviated upon IL-15 pretreatment, which enhanced mammalian target of rapamycin complex 1 (mTORC1) activity. IL-15 priming enhanced NK cell functionality to anti-CD16 stimulation in HIV-1 infection, representing an effective strategy for pharmacologically boosting NK cell responses.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.