Activation of MHC Class I, II, and CD40 Gene Expression by Histone Deacetylase Inhibitors
Open accessAbstract
Epigenetic mechanisms are involved in regulating chromatin structure and gene expression through repression. In this study, we show that histone deacetylase inhibitors (DAIs) that alter the acetylation of histones in chromatin enhance the expression of several genes on tumor cells including: MHC class I, II, and the costimulatory molecule CD40. Enhanced transcription results in a significant increase in protein expression on the tumor cell surface, and expression can be elicited on some tumors that are unresponsive to IFN-γ. The magnitude of induction of these genes cannot be explained by the effect of DAIs on the cell cycle or enhanced apoptosis. Induction of class II genes by DAIs was accompanied by activation of a repressed class II transactivator gene in a plasma cell tumor but, in several other tumor cell lines, class II was induced in the apparent absence of class II transactivator transcripts. These findings also suggest that the abnormalities observed in some tumors in the expression of genes critical to tumor immunity may result from epigenetic alterations in chromatin and gene regulation in addition to well-established mutational mechanisms.
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HDAC inhibitors changed immunogenicity and enhanced antitumor immunity via decreasing MDSC ratio and upregulating MHC-I/II, CD40, CD80, and CD86 expression.
“Beyond direct cytotoxicity, histone deacetylases (HDAC) inhibitors changed immunogenicity and enhanced antitumor immunity, via decreasing MDSC ratio and upregulating MHC-I/II, CD40, CD80, and CD86 expression [326–328].”
From Combination strategies with PD-1/PD-L1 blockade: current advances and future directions (2022) · cites this paper as [327]
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References 51 · Cited by 294
Research works printed but not linked: 1
- Stewart, C. C., and S. J. Stewart. 1997. Immunophenotyping. In Current Proto- cols in Cytometry, J. P. Robinson, Z. Darzynkiewicz, P. Dean, L. Dressler, P. Rabinovitch, C. Stewart, H. Tanke, and L. Wheeless, eds. Wiley, New York, p. 6.2.1-6.2.15.
- Authors
- Magner, W. J., Kazim, A. L., Stewart, C., Romano, M. A., Catalano, G., Grande, C., Keiser, N., Santaniello, F., & Tomasi, T. B.
- Affiliations
- Roswell Park Comprehensive Cancer Center (US)
- Corresponding author
- Catalano, Geoffrey
- Grande, Catherine
- Keiser, Nicholas
- Santaniello, Frank
- ORCID
- Magner, William J
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2000-12
- Volume
- 165
- Issue
- 12
- Pages
- 7017-7024
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W2159959495
- Cited by
- 294
- References
- 51
- Citations by year
- 2026: 6 · 2025: 11 · 2024: 10 · 2023: 18 · 2022: 14 · 2021: 15 · 2020: 13 · 2019: 10 · 2018: 12 · 2017: 18 · 2016: 22 · 2015: 10 · 2014: 11 · 2013: 15 · 2012: 8
- FWCI
- 2.53
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Cancer Institute (CA 16056., P30CA016056)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD017013, HD-17013)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Histone Deacetylase Inhibitors Research
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Keywords
- histone deacetylase inhibitors, MHC class I, MHC class II, CD40, epigenetic regulation, histone acetylation, chromatin structure, CIITA, plasma cell tumor, antitumor immunity, transcriptional activation
- MeSH terms
- Animals, Histocompatibility Antigens Class II, Cell Cycle, Chromatin, Enzyme Inhibitors, Gene Expression Regulation, Genes, MHC Class II, Genes, MHC Class I, Humans, Hydroxamic Acids, Interferon-gamma, Nuclear Proteins, RNA, Messenger, Tumor Cells, Cultured, Trans-Activators, Apoptosis, CD40 Antigens, Mice, Histone Deacetylase Inhibitors
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