ArticleOncoimmunology
Soluble NKG2D ligands in the ovarian cancer microenvironment are associated with an adverse clinical outcome and decreased memory effector T cells independent of NKG2D downregulation.
Article in Oncoimmunology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 41 citations in OpenAlex.
- Natural killer cells in ovarian cancer therapy: mechanisms, evasion, and therapeutic innovations.Inflammopharmacology · 2026Review
- Ascites reprograms innate lymphoid immune cells in ovarian cancer by promoting ILC2 enrichment and dysfunctional NK-cell states.Journal for immunotherapy of cancer · 2026Article
- Natural Killer Cell Plasticity in Epithelial Ovarian Cancer and Their Therapeutic Implications.Cells · 2026Review
- Immune Evasion in Ovarian Cancer Peritoneal Metastasis: Mechanisms and Biomarker-Guided Therapeutic Matching.Journal of cellular physiology · 2026Review
- Cell type-specific upregulation of NKG2D ligand MICA in response to APTO253.Annals of translational medicine · 2024Article
- Solid tumor immunotherapy using NKG2D-based adaptor CAR T cells.Cell reports. Medicine · 2024Article
- Arachidonic acid impairs natural killer cell functions by disrupting signaling pathways driven by activating receptors and reactive oxygen species.Cell communication and signaling : CCS · 2024Article
- Comprehensive snapshots of natural killer cells functions, signaling, molecular mechanisms and clinical utilization.Signal transduction and targeted therapy · 2024Review
- Review
- Article
- The emergence of DNAM-1 as the facilitator of NK cell-mediated killing in ovarian cancer.Frontiers in immunology · 2024Article
- TRAIL-dependent apoptosis of peritoneal mesothelial cells by NK cells promotes ovarian cancer invasion.iScience · 2023Article
- Electrolyte imbalance causes suppression of NK and T cell effector function in malignant ascites.Journal of experimental & clinical cancer research : CR · 2023Article
- Review
- Stem cell-assisted enzyme/prodrug therapy makes drug-resistant ovarian cancer cells vulnerable to natural killer cells through upregulation of NKG2D ligands.Medical oncology (Northwood, London, England) · 2023Article
- Arachidonic acid, a clinically adverse mediator in the ovarian cancer microenvironment, impairs JAK-STAT signaling in macrophages by perturbing lipid raft structures.Molecular oncology · 2022Article
- Recruited and Tissue-Resident Natural Killer Cells in the Lung During Infection and Cancer.Frontiers in immunology · 2022Review
- Role of Polymorphisms of NKG2D Receptor and Its Ligands in Acute Myeloid Leukemia and Human Stem Cell Transplantation.Frontiers in immunology · 2021Review
- Tumor-associated carbohydrates and immunomodulatory lectins as targets for cancer immunotherapy.Journal for immunotherapy of cancer · 2020Review
- Epithelial Ovarian Cancer and the Immune System: Biology, Interactions, Challenges and Potential Advances for Immunotherapy.Journal of clinical medicine · 2020Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The immune receptor NKG2D is predominantly expressed on NK cells and T cell subsets and confers anti-tumor activity. According to the current paradigm, immune surveillance is counteracted by soluble ligands shed into the microenvironment, which down-regulate NKG2D receptor expression. Here, we analyzed the clinical significance of the soluble NKG2D ligands sMICA and sULBP2 in the malignancy-associated ascites of ovarian cancer. We show that high levels of sMICA and sULBP2 in ascites were associated with a poor prognosis. Ascites inhibited the activation of normal NK cells, which, in contrast to the prevailing notion, was not associated with decreased NKG2D expression. Of note, an inverse correlation of soluble NKG2D ligands with effector memory T cells and a direct correlation with pro-tumorigenic CD163
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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.