ArticleNature communications2016
Melanoma cell lysosome secretory burst neutralizes the CTL-mediated cytotoxicity at the lytic synapse.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 70 citations in OpenAlex.
- Mechanisms of tumor cell evasion from NK cell-mediated killing and advances in NK cell-based cancer immunotherapy.Pharmaceutical science advances · 2026Review
- Unraveling Lysosomal Exocytosis: From Molecular Mechanisms to Physiological Functions.Traffic (Copenhagen, Denmark) · 2026Review
- Comprehensive characterization of lysosome-dependent cell death reveals prognostic significance and immune landscape in colon adenocarcinoma.Scientific reports · 2025Article
- Immunological synapse: structures, molecular mechanisms and therapeutic implications in disease.Signal transduction and targeted therapy · 2025Review
- Determinants of resistance and response to melanoma therapy.Nature cancer · 2024Review
- Autophagy: a necessary evil in cancer and inflammation.3 Biotech · 2024Review
- Is the tumor cell side of the immunological synapse a polarized secretory domain?Frontiers in immunology · 2024Article
- Extracellular vesicles and microvilli in the immune synapse.Frontiers in immunology · 2023Review
- Measuring CTL Lytic Granule Secretion and Target Cell Membrane Repair by Fluorescent Lipophilic Dye Uptake at the Lytic Synapse.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Irradiation combined with PD-L1iScience · 2022Article
- Review
- Enhancing CAR T function with the engineered secretion of C. perfringens neuraminidase.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Ultrarapid lytic granule release from CTLs activates CaScience advances · 2022Article
- Radiotherapy transiently reduces the sensitivity of cancer cells to lymphocyte cytotoxicity.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- The human cathelicidin peptide LL-37 inhibits pancreatic cancer growth by suppressing autophagy and reprogramming of the tumor immune microenvironment.Frontiers in pharmacology · 2022Article
- Escaping Death: How Cancer Cells and Infected Cells Resist Cell-Mediated Cytotoxicity.Frontiers in immunology · 2022Review
- Review
- Nature vs. Nurture: The Two Opposing Behaviors of Cytotoxic T Lymphocytes in the Tumor Microenvironment.International journal of molecular sciences · 2021Review
- The (re)discovery of tumor-intrinsic determinants of immune sensitivity by functional genetic screens.Immuno-oncology technology · 2021Review
- Cytotoxic T cells are able to efficiently eliminate cancer cells by additive cytotoxicity.Nature communications · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human melanoma cells express various tumour antigens that are recognized by CD8(+) cytotoxic T lymphocytes (CTLs) and elicit tumour-specific responses in vivo. However, natural and therapeutically enhanced CTL responses in melanoma patients are of limited efficacy. The mechanisms underlying CTL effector phase failure when facing melanomas are still largely elusive. Here we show that, on conjugation with CTL, human melanoma cells undergo an active late endosome/lysosome trafficking, which is intensified at the lytic synapse and is paralleled by cathepsin-mediated perforin degradation and deficient granzyme B penetration. Abortion of SNAP-23-dependent lysosomal trafficking, pH perturbation or impairment of lysosomal proteolytic activity restores susceptibility to CTL attack. Inside the arsenal of melanoma cell strategies to escape immune surveillance, we identify a self-defence mechanism based on exacerbated lysosome secretion and perforin degradation at the lytic synapse. Interfering with this synaptic self-defence mechanism might be useful in potentiating CTL-mediated therapies in melanoma patients.
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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.