ArticleCancer immunology, immunotherapy : CII2016
Histone deacetylase inhibitors enhance CD1d-dependent NKT cell responses to lymphoma.
Article in Cancer immunology, immunotherapy : CII, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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
20 citing papers in PubMed, 30 citations in OpenAlex.
- Review
- Epigenetic control ofFrontiers in immunology · 2023Article
- Immune-epigenetic crosstalk in haematological malignancies.Frontiers in cell and developmental biology · 2023Review
- The function of histone methylation and acetylation regulators in GBM pathophysiology.Frontiers in oncology · 2023Review
- Research progress on epigenetics of small B-cell lymphoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Review
- Insights into the therapeutic potential of histone deacetylase inhibitor/immunotherapy combination regimens in solid tumors.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Review
- Review
- Review
- Epigenetic Mechanisms of Resistance to Immune Checkpoint Inhibitors.Biomolecules · 2020Review
- HDAC inhibitors overcome immunotherapy resistance in B-cell lymphoma.Protein & cell · 2020Review
- Natural Products Impacting DNA Methyltransferases and Histone Deacetylases.Frontiers in pharmacology · 2020Review
- Emerging epigenetic-modulating therapies in lymphoma.Nature reviews. Clinical oncology · 2019Review
- Unconventional Approaches to Modulating the Immunogenicity of Tumor Cells.Advances in cancer research · 2018Review
- CD1d-Invariant Natural Killer T Cell-Based Cancer Immunotherapy: α-Galactosylceramide and Beyond.Frontiers in immunology · 2018Review
- Trichostatin A and 5-Aza-2'-Deoxycytidine influence the expression of cold-induced genes in Arabidopsis.Plant signaling & behavior · 2017Article
- HDAC4 is expressed on multiple T cell lineages but dispensable for their development and function.Oncotarget · 2017Article
- Harnessing the Power of Invariant Natural Killer T Cells in Cancer Immunotherapy.Frontiers in immunology · 2017Review
- Is There an Opportunity for Current Chemotherapeutics to Up-regulate MIC-A/B Ligands?Frontiers in pharmacology · 2017Article
- Epi-drugs in combination with immunotherapy: a new avenue to improve anticancer efficacy.Clinical epigenetics · 2017Review
- Trichostatin A Sensitizes Hepatocellular Carcinoma Cells to Enhanced NK Cell-mediated Killing by Regulating Immune-related Genes.Cancer genomics & proteomicsArticle
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Histone deacetylases (HDACs) are a family of enzymes that influence expression of genes implicated in tumor initiation, progression, and anti-tumor responses. In addition to their canonical role in deacetylation of histones, HDACs regulate many non-canonical targets, such as Signal Transducer and Activator of Transcription 3 (STAT3). We hypothesize that tumors use epigenetic mechanisms to dysregulate CD1d-mediated antigen presentation, thereby impairing the ability of natural killer T (NKT) cells to recognize and destroy malignant cells. In this study, we pre-treated CD1d-expressing tumor cells with HDAC inhibitors (HDACi) and assessed CD1d-dependent NKT cell responses to mantle cell lymphoma (MCL). Pre-treatment with Trichostatin-A, a pan-HDACi, rapidly enhanced both CD1d- and MHC class II-mediated antigen presentation. Similarly, treatment of MCL cells with other HDACi resulted in enhanced CD1d-dependent NKT cell responses. The observed changes are due, at least in part, to an increase in both CD1D mRNA and CD1d cell surface expression. Mechanistically, we found that HDAC2 binds to the CD1D promoter. Knockdown of HDAC2 in tumor cells resulted in a significant increase in CD1d-mediated antigen presentation. In addition, treatment with HDACi inhibited STAT3 and STAT3-regulated inflammatory cytokine secretion by MCL cells. We demonstrated that MCL-secreted IL-10 inhibits CD1d-mediated antigen presentation and pre-treatment with TSA abrogates secretion of IL-10 by MCL. Taken together, our studies demonstrate the efficacy of HDACi in restoring anti-tumor responses to MCL through both cell-intrinsic and cell-extrinsic mechanisms and strongly implicate a role for HDACi in enhancing immune responses to cancer.
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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.