ArticleOncotarget2015
Regulation of split anergy in natural killer cells by inhibition of cathepsins C and H and cystatin F.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- Transcriptomic Profiling Identifies Neutrophil-Specific Upregulation of Cystatin F as a Marker of Acute Inflammation in Humans.Frontiers in immunology · 2021Pooled it
- Preventing trogocytosis by cathepsin B inhibition augments CAR T-cell function.Signal transduction and targeted therapy · 2026Article
- Review
- Preventing trogocytosis by cathepsin B inhibition augments CAR T cell function.bioRxiv : the preprint server for biology · 2025Article
- Cystatin F-a key player in central nervous system disease.Journal of neuroinflammation · 2025Review
- The diversity of natural killer cell functional and phenotypic states in cancer.Cancer metastasis reviews · 2025Review
- Targeting cystatin F activation enhances NK cell cytotoxicity in glioblastoma models.Frontiers in immunology · 2025Article
- Cystatin F Depletion inInternational journal of molecular sciences · 2024Article
- Deciphering Tumor Cell Evolution in Cutaneous T-Cell Lymphomas: Distinct Differentiation Trajectories in Mycosis Fungoides and Sézary Syndrome.The Journal of investigative dermatology · 2024Article
- Different glycosylation profiles of cystatin F alter the cytotoxic potential of natural killer cells.Cellular and molecular life sciences : CMLS · 2023Article
- Type 2 Cystatins and Their Roles in the Regulation of Human Immune Response and Cancer Progression.Cancers · 2023Review
- Article
- Cysteine Cathepsins as Therapeutic Targets in Immune Regulation and Immune Disorders.Biomedicines · 2023Review
- What is the Potential Interplay between Microbiome and Tumor Microenvironment in Oral Squamous Cell Carcinomas?Asian Pacific journal of cancer prevention : APJCP · 2022Review
- Lysosomal peptidases-intriguing roles in cancer progression and neurodegeneration.FEBS open bio · 2022Review
- Helicobacter pylori and gastric cancer: a lysosomal protease perspective.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2022Review
- New inhibitors of cathepsin V impair tumor cell proliferation and elastin degradation and increase immune cell cytotoxicity.Computational and structural biotechnology journal · 2022Article
- Glycosylated Cathepsin V Serves as a Prognostic Marker in Lung Cancer.Frontiers in oncology · 2022Article
- Proteases Regulate Cancer Stem Cell Properties and Remodel Their Microenvironment.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2021Review
- Cystatin F acts as a mediator of immune suppression in glioblastoma.Cellular oncology (Dordrecht, Netherlands) · 2021Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Freshly isolated human primary NK cells induce preferential lysis of Oral Squamous Carcinoma Stem Cells (OSCSCs) when compared to differentiated Oral Squamous Carcinoma Cells (OSCCs), while anti-CD16 antibody and monocytes induce functional split anergy in primary NK cells by decreasing the cytotoxic function of NK cells and increasing the release of IFN-γ. Since NK92 cells have relatively lower levels of cytotoxicity when compared to primary NK cells, and have the ability to increase secretion of regulatory cytokines IL-10 and IL-6, we used these cells as a model of NK cell anergy to identify and to study the upstream regulators of anergy. We demonstrate in this paper that the levels of truncated monomeric cystatin F, which is known to inhibit the functions of cathepsins C and H, is significantly elevated in NK92 cells and in anergized primary NK cells. Furthermore, cystatin F co-localizes with cathepsins C and H in the lysosomal/endosomal vesicles of NK cells. Accordingly, the mature forms of aminopeptidases cathepsins C and H, which regulate the activation of effector granzymes in NK cells, are significantly decreased, whereas the levels of pro-cathepsin C enzyme is increased in anergized NK cells after triggering of the CD16 receptor. In addition, the levels of granzyme B is significantly decreased in anti-CD16mAb and target cell anergized primary NK cells and NK92 cells. Our study provides the cellular and molecular mechanisms by which target cells may utilize to inhibit the cytotoxic function of NK cells.
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Registered trials
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