ArticleJournal of virology2013
KLRG1 negatively regulates natural killer cell functions through the Akt pathway in individuals with chronic hepatitis C virus infection.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.
- Genetically adjusted PSA levels for prostate cancer screening.Nature medicine · 2023Pooled it
- MicroRNA-155 regulates interferon-γ production in natural killer cells via Tim-3 signalling in chronic hepatitis C virus infection.Immunology · 2015Trial
- Single-cell landscape of peripheral and tumor-infiltrating immune cells in HPV-negative HNSCC.Oncoimmunology · 2026Article
- The suppressive function of ILC2 cells is regulated by β2-adrenergic receptor signaling in breast cancer.NPJ breast cancer · 2026Article
- KLRG1 silencing increases the efficacy of CAR NK cell therapy against colon cancer via SHP-2/ZAP-70/NF-κB signal pathway.Journal of translational medicine · 2026Article
- Sialylation in Colorectal Cancer Rewires Antitumor Immunity at the Peritoneal Metastatic Site.European journal of immunology · 2026Article
- The dual roles of natural killer cells in liver immunity and tolerance: Implications for health and disease.Hepatology communications · 2026Review
- Association between T cell exhaustion and the recurrence of atrial fibrillation after cryoballoon ablation.Frontiers in immunology · 2026Article
- Parental clinical manifestation association with newborn immune senescence and telomere biology in Pakistan.BMC research notes · 2025Article
- Review
- KLRG1 expression induces functional exhaustion of NK cells in colorectal cancer patients.Cancer immunology, immunotherapy : CII · 2025Article
- NK Cell Senescence in Cancer: From Molecular Mechanisms to Therapeutic Opportunities.Aging and disease · 2025Review
- A ligand-centered framework for γδ T cell activation in colorectal cancer revealed by single-cell and transformer-based perturbation.Frontiers in immunology · 2025Article
- Article
- The role of KLRG1: a novel biomarker and new therapeutic target.Cell communication and signaling : CCS · 2024Review
- Persistence of a Skewed Repertoire of NK Cells in People with HIV-1 on Long-Term Antiretroviral Therapy.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- BET inhibitors drive Natural Killer activation in non-small cell lung cancer via BRD4 and SMAD3.Nature communications · 2024Article
- Article
- Reliable Hallmarks and Biomarkers of Senescent Lymphocytes.International journal of molecular sciences · 2023Review
- KLRG1 expression on natural killer cells is associated with HIV persistence, and its targeting promotes the reduction of the viral reservoir.Cell reports. Medicine · 2023Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
In this study, we demonstrate that killer cell lectin-like receptor subfamily G member 1 (KLRG1), a transmembrane protein preferentially expressed on T cells, is highly expressed on CD56(+) NK cells, which are significantly reduced in their numbers and functions in the peripheral blood of patients with chronic hepatitis C virus (HCV) infection compared to subjects without infection. KLRG1 expression is also upregulated on healthy NK cells exposed to Huh-7 hepatocytes infected with HCV in vitro. Importantly, the expression levels of KLRG1 are inversely associated with the capacity of NK cells to proliferate and to produce gamma interferon (IFN-γ) but positively associated with apoptosis of NK cells in response to inflammatory cytokine stimulation. KLRG1(+) NK cells, including CD56(bright) and CD56(dim) subsets, exhibit impaired cell activation and IFN-γ production but increased apoptosis compared to KLRG1(-) NK cells, particularly in HCV-infected individuals. Importantly, blockade of KLRG1 signaling significantly recovered the impaired IFN-γ production by NK cells from HCV-infected subjects. Blockade of KLRG1 also enhanced the impaired phosphorylation of Akt (Ser473) in NK cells from HCV-infected subjects. Taken together, these results indicate that KLRG1 negatively regulates NK cell numbers and functions via the Akt pathway, thus providing a novel marker and therapeutic target for HCV infection.
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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.