ArticlePLoS pathogens2016
A Conserved HIV-1-Derived Peptide Presented by HLA-E Renders Infected T-cells Highly Susceptible to Attack by NKG2A/CD94-Bearing Natural Killer Cells.
Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 85 citations in OpenAlex.
- Constitutive natural killer cell features associated with post-treatment control of SIV infection in the pVISCONTI study.Nature communications · 2026Article
- HIV tri-specific killer engagers directly enhance NK cell function and safely expand NK cells in vivo.Cell reports. Medicine · 2026Article
- CD56bioRxiv : the preprint server for biology · 2026Article
- Retinoids enhance NK effector function against HIV-infected CD4 T cells.Journal of virology · 2026Article
- Immune correlates of HIV-1 rebound during broadly neutralizing antibody treatment in young children.The Journal of clinical investigation · 2026Article
- NK Cells Engineered with a Chimeric Antigen Receptor Delay HIV Rebound and Reshape HIV Reservoir Composition.bioRxiv : the preprint server for biology · 2026Article
- Targeting MHC-E as a new strategy for vaccines and immunotherapeutics.Nature reviews. Immunology · 2026Review
- The Expanding Role of HLA-E in Host Defense: A Target for Broadly Applicable Vaccines and Immunotherapies.Cells · 2025Review
- NKp30 and NKG2D contribute to natural killer cell-mediated recognition of HIV-infected cells.iScience · 2025Article
- Sex differences in HIV-1 reservoir cell selection are linked to altered innate immune profiles.Science translational medicine · 2025Observational
- Dual Role of Natural Killer Cells in Early Pregnancy: Immunopathological Implications and Therapeutic Potential in Recurrent Spontaneous Abortion and Recurrent Implantation Failure.Cell proliferation · 2025Review
- Impact of the IL-15 superagonist N-803 on lymphatic reservoirs of HIV.JCI insight · 2025Article
- Hantaan virus-derived peptides that stabilize HLA-E could abrogate inhibition of CD56dimNKG2A+ NK cells.PLoS pathogens · 2025Article
- Emerging mutation in SARS-CoV-2 facilitates escape from NK cell recognition and associates with enhanced viral fitness.PLoS pathogens · 2024Article
- Review
- NKG2C and NKG2A coexpression defines a highly functional antiviral NK population in spontaneous HIV control.JCI insight · 2024Article
- HIV-1 control in vivo is related to the number but not the fraction of infected cells with viral unspliced RNA.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Enhancing Therapeutic Efficacy of FLT3 Inhibitors with Combination Therapy for Treatment of Acute Myeloid Leukemia.International journal of molecular sciences · 2024Review
- HIV-1 control in vivo is related to the number but not the fraction of infected cells with viral unspliced RNA.bioRxiv : the preprint server for biology · 2024Article
- Obtaining Gene-Modified HLA-E-Expressing Feeder Cells for Stimulation of Natural Killer Cells.Pharmaceutics · 2024Article
10 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
Major histocompatibility class I (MHC-I)-specific inhibitory receptors on natural killer (NK) cells (iNKRs) tolerize mature NK cell responses toward normal cells. NK cells generate cytolytic responses to virus-infected or malignant target cells with altered or decreased MHC-I surface expression due to the loss of tolerizing ligands. The NKG2A/CD94 iNKR suppresses NK cell responses through recognition of the non-classical MHC-I, HLA-E. We used HIV-infected primary T-cells as targets in an in vitro cytolytic assay with autologous NK cells from healthy donors. In these experiments, primary NKG2A/CD94(+) NK cells surprisingly generated the most efficient responses toward HIV-infected T-cells, despite high HLA-E expression on the infected targets. Since certain MHC-I-presented peptides can alter recognition by iNKRs, we hypothesized that HIV-1-derived peptides presented by HLA-E on infected cells may block engagement with NKG2A/CD94, thereby engendering susceptibility to NKG2A/CD94(+) NK cells. We demonstrate that HLA-E is capable of presenting a highly conserved peptide from HIV-1 capsid (AISPRTLNA) that is not recognized by NKG2A/CD94. We further confirmed that HLA-C expressed on HIV-infected cells restricts attack by KIR2DL(+) CD56(dim) NK cells, in contrast to the efficient responses by CD56(bright) NK cells, which express predominantly NKG2A/CD94 and lack KIR2DLs. These findings are important since the use of NK cells was recently proposed to treat latently HIV-1-infected patients in combination with latency reversing agents. Our results provide a mechanistic basis to guide these future clinical studies, suggesting that ex vivo-expanded NKG2A/CD94(+) KIR2DL(-) NK cells may be uniquely beneficial.
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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.