ArticleInternational journal of medical sciences2015
Effect of helixor A on natural killer cell activity in endometriosis.
Article in International journal of medical sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 25 citations in OpenAlex.
- Immune escape in endometriosis: mechanisms, reprogramming strategies, and precision interventions.Reproductive biology and endocrinology : RB&E · 2026Review
- Endometriosis immune microenvironment timing shifts: from immune escape to immune exhaustion.Cell death discovery · 2026Review
- Shared diagnostic biomarkers and underlying mechanisms between endometriosis and recurrent implantation failure.Frontiers in endocrinology · 2025Article
- Dysfunction of natural killer cells promotes immune escape and disease progression in endometriosis.Frontiers in immunology · 2025Review
- Immune micro-environment analysis and drug screening for ovarian endometriosis.Genes & genomics · 2024Article
- Immune pathway through endometriosis to ovarian cancer.World journal of clinical oncology · 2024Review
- Immunotherapy: A promising novel endometriosis therapy.Frontiers in immunology · 2023Review
- Diagnostic gene biomarkers for predicting immune infiltration in endometriosis.BMC women's health · 2022Article
- Effect of combined contraceptive pill on immune cell of ovarian endometriotic tissue.Journal of ovarian research · 2021Article
- Increased Levels of CD107a and Intracellular Cytokines in IL-2 Stimulated PBMCs from Endometriosis Patients.International journal of inflammation · 2021Article
- NK Cells as Potential Targets for Immunotherapy in Endometriosis.Journal of clinical medicine · 2019Review
- Decreased Cytotoxicity of Peripheral and Peritoneal Natural Killer Cell in Endometriosis.BioMed research international · 2016Review
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
aimNK cells are one of the major immune cells in endometriosis pathogenesis. While previous clinical studies have shown that helixor A to be an effective treatment for endometriosis, little is known about its mechanism of action, or its relationship with immune cells. The aim of this study is to investigate the effects of helixor A on Natural killer cell (NK cell) cytotoxicity in endometriosis MATERIALS AND
methodsWe performed an experimental study. Samples of peritoneal fluid were obtained from January 2011 to December 2011 from 50 women with endometriosis and 50 women with other benign ovarian cysts (control). Peritoneal fluid of normal control group and endometriosis group was collected during laparoscopy. Baseline cytotoxicity levels of NK cells were measured with the peritoneal fluid of control group and endometriosis group. Next, cytotoxicity of NK cells was evaluated before and after treatment with helixor A. NK-cell activity was determined based upon the expression of CD107a, as an activation marker.
resultsNK cells cytotoxicity was 79.38±2.13% in control cells, 75.55±2.89% in the control peritoneal fluid, 69.59±4.96% in endometriosis stage I/II endometriosis, and 63.88±5.75% in stage III/IV endometriosis. A significant difference in cytotoxicity was observed between the control cells and stage III/IV endometriosis, consistent with a significant decrease in the cytotoxicity of NK cells in advanced stages of endometriosis; these levels increased significantly after treatment with helixor A; 78.30% vs. 86.40% (p=0.003) in stage I/II endometriosis, and 73.67% vs. 84.54% (p=0.024) in stage III/IV. The percentage of cells expressing CD107a was increased significantly in each group after helixor A treatment; 0.59% vs. 1.10% (p=0.002) in stage I/II endometriosis, and 0.79% vs. 1.40% (p=0.014) in stage III/IV.
conclusionsHelixor A directly influenced NK-cell cytotoxicity through direct induction of CD107a expression. Our results open new role of helixor A as an imune modulation therapy, or in combination with hormonal agents, for the treatment of endometriosis.
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