ArticleProceedings of the National Academy of Sciences of the United States of America2013
Natural killer cells in HIV controller patients express an activated effector phenotype and do not up-regulate NKp44 on IL-2 stimulation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 81 citations in OpenAlex.
- Early immune responses anticipate HIV rebound and precede viral control.bioRxiv : the preprint server for biology · 2026Article
- CXCR6Frontiers in immunology · 2026Article
- HIV-2 infection as a comparative lens for functional HIV-1 remission.Frontiers in immunology · 2026Review
- Persistent Type I Interferon Signaling Impairs Innate Lymphoid Cells During HIV-1 Infection Under Suppressive ART.Viruses · 2025Article
- Innate immune dysfunction and persistent activation in South African HIV elite controllers.Frontiers in immunology · 2025Article
- Genetically defined causal effects of natural killer cells related traits in risk of infection: a Mendelian randomization study.BMC infectious diseases · 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
- 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
- IL-15-dependent immune crosstalk between natural killer cells and dendritic cells in HIV-1 elite controllers.Cell reports · 2023Article
- HIV post-treatment controllers have distinct immunological and virological features.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Bibliometric and visualized analysis of elite controllers based on CiteSpace: landscapes, hotspots, and frontiers.Frontiers in cellular and infection microbiology · 2023Article
- Article
- Immune correlates of HIV-1 reservoir cell decline in early-treated infants.Cell reports · 2022Article
- Persistence of Unintegrated HIV DNA Associates With Ongoing NK Cell Activation and CD34+DNAM-1brightCXCR4+ Precursor Turnover in Vertically Infected Patients Despite Successful Antiretroviral Treatment.Frontiers in immunology · 2022Article
- Prime, shock and kill: BCL-2 inhibition for HIV cure.Frontiers in immunology · 2022Review
- NK Cells, Monocytes and Macrophages in HIV-1 Control: Impact of Innate Immune Responses.Frontiers in immunology · 2022Review
- Learning to Be Elite: Lessons From HIV-1 Controllers and Animal Models on Trained Innate Immunity and Virus Suppression.Frontiers in immunology · 2022Review
- The Role of Innate Immunity in Natural Elite Controllers of HIV-1 Infection.Frontiers in immunology · 2022Review
- The Longest Persistence of Viable SARS-CoV-2 With Recurrence of Viremia and Relapsing Symptomatic COVID-19 in an Immunocompromised Patient-A Case Study.Open forum infectious diseases · 2021Article
- Siglec-9 defines and restrains a natural killer subpopulation highly cytotoxic to HIV-infected cells.PLoS pathogens · 2021Article
Corrections and comments
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Authors and funding
16 authors at 9 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Control of HIV replication in elite controller (EC) and long-term nonprogressor (LTNP) patients has been associated with efficient CD8(+)cytotoxic T-lymphocyte function. However, innate immunity may play a role in HIV control. We studied the expression of natural cytotoxicity receptors (NKp46, NKp30, and NKp44) and their induction over a short time frame (2-4 d) on activation of natural killer (NK) cells in 31 HIV controller patients (15 ECs, 16 LTNPs). In EC/LTNP, induction of NKp46 expression was normal but short (2 d), and NKp30 was induced to lower levels vs. healthy donors. Notably, in antiretroviral-treated aviremic progressor patients (TAPPs), no induction of NKp46 or NKp30 expression occurred. More importantly, EC/LTNP failed to induce expression of NKp44, a receptor efficiently induced in activated NK cells in TAPPs. The specific lack of NKp44 expression resulted in sharply decreased capability of killing target cells by NKp44, whereas TAPPs had conserved NKp44-mediated lysis. Importantly, conserved NK cell responses, accompanied by a selective defect in the NKp44-activating pathway, may result in lack of killing of uninfected CD4(+)NKp44Ligand(+) cells when induced by HIVgp41 peptide-S3, representing a relevant mechanism of CD4(+) depletion. In addition, peripheral NK cells from EC/LTNP had increased NKG2D expression, significant HLA-DR up-regulation, and a mature (NKG2A-CD57(+)killer cell Ig-like receptor(+)CD85j(+)) phenotype, with cytolytic function also against immature dendritic cells. Thus, NK cells in EC/LTNP can maintain substantially unchanged functional capabilities, whereas the lack of NKp44 induction may be related to CD4 maintenance, representing a hallmark of these patients.
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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.