ArticleProceedings of the National Academy of Sciences of the United States of America2019
IL-17 constrains natural killer cell activity by restraining IL-15-driven cell maturation via SOCS3.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 41 citations in OpenAlex.
- Armed Oncolytic Myxoma Virus Induces Systemic Antitumor Immunity Against Solid Tumors in Immunocompetent Mice.Research square · 2026Article
- Function-driven design of a surrogate interleukin-2 receptor ligand.FEBS letters · 2026Article
- SOCS3: An Immunological Biomarker Offering Potential Therapeutic Targets for Malignant Tumors.Biological procedures online · 2025Review
- Conserved functional features of natural killer cell subsets in chicken, human, and murine immune systems.iScience · 2025Article
- Cartilage decellularized matrix hydrogel loaded with protocatechualdehyde for targeted epiphycan treatment of osteoarthritis.Materials today. Bio · 2024Article
- IL-15 in T-Cell Responses and Immunopathogenesis.Immune network · 2024Review
- The synergistic effects of anoikis-related genes and EMT-related genes in the prognostic prediction of Wilms tumor.Frontiers in molecular biosciences · 2024Article
- Exhausted signature and regulatory network of NK cells in myasthenia gravis.Frontiers in immunology · 2024Article
- Cellular interactions in tumor microenvironment during breast cancer progression: new frontiers and implications for novel therapeutics.Frontiers in immunology · 2024Review
- Natural killer cells in the lung: potential role in asthma and virus-induced exacerbation?European respiratory review : an official journal of the European Respiratory Society · 2023Review
- Current status and future perspective of natural killer cell therapy for cancer.Medical review (2021) · 2023Review
- T cells in health and disease.Signal transduction and targeted therapy · 2023Review
- Immature natural killer cells promote progression of triple-negative breast cancer.Science translational medicine · 2023Article
- Interleukin-17 signaling influences CD8Oncoimmunology · 2023Article
- NK cell exhaustion in the tumor microenvironment.Frontiers in immunology · 2023Review
- Article
- IL-17A Mediates Demyelination by Activating A1 AstrocytesFrontiers in immunology · 2022Article
- Cross-Platform in-silico Analyses Exploring Tumor Immune Microenvironment with Prognostic Value in Triple-Negative Breast Cancer.Breast cancer (Dove Medical Press) · 2022Article
- Stem cells-derived natural killer cells for cancer immunotherapy: current protocols, feasibility, and benefits of ex vivo generated natural killer cells in treatment of advanced solid tumors.Cancer immunology, immunotherapy : CII · 2021Review
- TIPE2 is a checkpoint of natural killer cell maturation and antitumor immunity.Science advances · 2021Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increasing evidence demonstrates that IL-17A promotes tumorigenesis, metastasis, and viral infection. Natural killer (NK) cells are critical for defending against tumors and infections. However, the roles and mechanisms of IL-17A in regulating NK cell activity remain elusive. Herein, our study demonstrated that IL-17A constrained NK cell antitumor and antiviral activity by restraining NK cell maturation. It was observed that the development and metastasis of tumors were suppressed in IL-17A-deficient mice in the NK cell-dependent manner. In addition, the antiviral activity of NK cells was also improved in IL-17A-deficient mice. Mechanistically, ablation of IL-17A signaling promoted generation of terminally mature CD27
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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.