ArticleJournal of virology2009
Activation of natural killer cells by newcastle disease virus hemagglutinin-neuraminidase.
Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers.
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Who cites it
105 citing papers in PubMed, 166 citations in OpenAlex.
- Ex vivo evaluation of Newcastle disease virus to enhance natural killer cell function against acute myeloid leukemia cells.Scientific reports · 2026Article
- Gamma-irradiated Newcastle disease virus: an alternative inactivated oncolytic virotherapy.Immunology and cell biology · 2026Article
- Newcastle Disease Virus - Induced Interferons Regulate PD-L1 and MICA Expression in Human Tumor and Normal Cells.ImmunoTargets and therapy · 2026Article
- Natural killer cell activated by attenuated newcastle disease virus (NDV) as anti-cancer therapy.Frontiers in molecular biosciences · 2026Article
- Engineering the tumor microenvironment: oncolytic NDV to facilitate CAR-T cell therapy.Journal of translational medicine · 2025Review
- Review
- Review
- ITAM-based receptors in natural killer cells.Immunological reviews · 2024Review
- Article
- Unraveling the dynamic mechanisms of natural killer cells in viral infections: insights and implications.Virology journal · 2024Review
- Review of cancer therapies for the perioperative physician.Perioperative medicine (London, England) · 2023Review
- Inhibition of Tumor Growth and Metastasis by Newcastle Disease Virus Strain P05 in a Breast Cancer Mouse Model.Journal of breast cancer · 2023Article
- Immune responses elicited by ssRNA(-) oncolytic viruses in the host and in the tumor microenvironment.Journal of cancer metastasis and treatment · 2023Article
- Direct interaction of the molecular chaperone GRP78/BiP with the Newcastle disease virus hemagglutinin-neuraminidase protein plays a vital role in viral attachment to and infection of culture cells.Frontiers in immunology · 2023Article
- Counteracting Immunosuppression in the Tumor Microenvironment by Oncolytic Newcastle Disease Virus and Cellular Immunotherapy.International journal of molecular sciences · 2022Review
- Avian Paramyxovirus 4 Antitumor Activity Leads to Complete Remissions and Long-term Protective Memory in Preclinical Melanoma and Colon Carcinoma Models.Cancer research communications · 2022Article
- Blocking the PCNA/NKp44 Checkpoint to Stimulate NK Cell Responses to Multiple Myeloma.International journal of molecular sciences · 2022Article
- Molecular Mechanisms of Anti-Neoplastic and Immune Stimulatory Properties of Oncolytic Newcastle Disease Virus.Biomedicines · 2022Review
- Activating Natural Killer Cell Receptors, Selectins, and Inhibitory Siglecs Recognize Ebolavirus Glycoprotein.Journal of innate immunity · 2022Article
- Review
45 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The avian paramyxovirus Newcastle disease virus (NDV) selectively replicates in tumor cells and is known to stimulate T-cell-, macrophage-, and NK cell-mediated responses. The mechanisms of NK cell activation by NDV are poorly understood so far. We studied the expression of ligand structures for activating NK cell receptors on NDV-infected tumor cells. Upon infection with the nonlytic NDV strain Ulster and the lytic strain MTH-68/H, human carcinoma and melanoma cells showed enhanced expression of ligands for the natural cytotoxicity receptors NKp44 and NKp46, but not NKp30. Ligands for the activating receptor NKG2D were partially downregulated. Soluble NKp44-Fc and NKp46-Fc, but not NKp30-Fc, chimeric proteins bound specifically to NDV-infected tumor cells and to NDV particle-coated plates. Hemagglutinin-neuraminidase (HN) of the virus serves as a ligand structure for NKp44 and NKp46, as indicated by the blockade of binding to NDV-infected cells and viral particles in the presence of anti-HN antibodies and by binding to cells transfected with HN cDNA. Consistent with the recognition of sialic acid moieties by the viral lectin HN, the binding of NKp44-Fc and NKp46-Fc was lost after desialylation. NKp44- and NKp46-CD3zeta lacZ-inducible reporter cells were activated by NDV-infected cells. NDV-infected tumor cells stimulated NK cells to produce increased amounts of the effector lymphokines gamma interferon and tumor necrosis factor alpha. Primary NK cells and the NK line NK-92 lysed NDV-infected tumor cells with enhanced efficiency, an effect that was eliminated by the treatment of target cells with the neuraminidase inhibitor Neu5Ac2en. These results suggest that direct activation of NK cells contributes to the antitumor effects of NDV.
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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.