ArticleCellular immunology2011
Enhancement of HLA class II-restricted CD4+ T cell recognition of human melanoma cells following treatment with bryostatin-1.
Article in Cellular immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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.
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Who cites it
18 citing papers in PubMed, 23 citations in OpenAlex.
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- Bioinformatic characterization of STING expression in hematological malignancies reveals association with prognosis and anti-tumor immunity.Frontiers in immunology · 2025Article
- Induction of Neural Differentiation and Protection by a Novel Slow-Release Nanoparticle Estrogen Construct in a Rat Model of Spinal Cord Injury.Neurochemical research · 2024Article
- GILT Expression in Human Melanoma Cells Enhances Generation of Antigenic Peptides for HLA Class II-Mediated Immune Recognition.International journal of molecular sciences · 2022Article
- Protective Effects of Estrogen via Nanoparticle Delivery to Attenuate Myelin Loss and Neuronal Death after Spinal Cord Injury.Neurochemical research · 2021Article
- Enolase inhibition alters metabolic hormones and inflammatory factors to promote neuroprotection in spinal cord injury.Neurochemistry international · 2020Article
- Latency reversal agents modulate HIV antigen processing and presentation to CD8 T cells.PLoS pathogens · 2020Article
- Autophagy-dependent crosstalk between GILT and PAX-3 influences radiation sensitivity of human melanoma cells.Journal of cellular biochemistry · 2018Article
- Diverse Impacts of HIV Latency-Reversing Agents on CD8+ T-Cell Function: Implications for HIV Cure.Frontiers in immunology · 2018Review
- Targeting Enolase in Reducing Secondary Damage in Acute Spinal Cord Injury in Rats.Neurochemical research · 2017Article
- Cell Signaling Pathways That Regulate Antigen Presentation.Journal of immunology (Baltimore, Md. : 1950) · 2016Review
- Bryostatin-1 causes radiosensitization of BMG-1 malignant glioma cells through differential activation of protein kinase-Cδ not evident in the non-malignant AA8 fibroblasts.Molecular and cellular biochemistry · 2015Article
- Elevation of c-MYC disrupts HLA class II-mediated immune recognition of human B cell tumors.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Reduction of myeloid-derived suppressor cells and lymphoma growth by a natural triterpenoid.Journal of cellular biochemistry · 2015Article
- Article
- A possible cross-talk between autophagy and apoptosis in generating an immune response in melanoma.Apoptosis : an international journal on programmed cell death · 2012Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
The majority of melanoma cells express detectable levels of HLA class II proteins, and an increased threshold of cell surface class II is crucial for the stimulation of CD4+ T cells. Bryostatin-1, a protein kinase C (PKC) activator, has been considered as a potent chemotherapeutic agent in a variety of in vitro tumor models. Little is known about the role of bryostatin-1 in HLA class II Ag presentation and immune activation in malignant tumors, especially in melanoma. In this study, we show that bryostatin-1 treatment enhances CD4+ T cell recognition of melanoma cells in the context of HLA class II molecules. We also show that bryostatin-1 treatment of melanoma cells increases class II protein levels by upregulating the class II transactivator (CIITA) gene. Flow cytometry and confocal microscopic analyses revealed that bryostatin-1 treatment upregulated the expression of costimulatory molecules (CD80 and CD86) in melanoma cells, which could prolong the interaction of immune cells and tumors. Bryostatin-1 also induced cellular differentiation in melanoma cells, and reduced tumorigenic factors such as pro-cathepsins and matrix-metalloproteinase-9. These data suggest that bryostatin-1 could be used as a chemo-immunotherapeutic agent for reducing tumorigenic potential of melanoma cells while enhancing CD4+ T cell recognition to prevent tumor recurrence.
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Registered trials
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.