T cells lacking HDAC11 have increased effector functions and mediate enhanced alloreactivity in a murine model
Open accessAbstract
gene promoters in resting T cells, where it rapidly disassociated following T-cell activation. In vivo, HDAC11KO T cells were refractory to tolerance induction. HDAC11KO T cells also mediated accelerated onset of acute graft-versus-host disease (GVHD) in a murine model, characterized by increased proliferation of T cells and expression of interferon-γ, tumor necrosis factor, and EOMES. In addition, adoptive transfer of HDAC11KO T cells resulted in significantly reduced tumor burden in a murine B-cell lymphoma model. Taken together, these data demonstrate a previously unknown role of HDAC11 as a negative epigenetic regulator of T-cell effector phenotype and function.
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In a B-cell lymphoma model, mice receiving T cells from Hdac11 KO donors show delayed tumor growth.
“In a B-cell lymphoma model, mice receiving T cells from Hdac11 KO donors show delayed tumor growth (Woods et al., 2017).”
From HDACs and the epigenetic plasticity of cancer cells: target the complexity (2022) · cites this paper as Woods et al., 2017
Tbet and Eomes are important regulators of inflammatory cytokines and effector molecules production.
“Hdac11 binds to promoters and represses transcription of TFs Tbet and Eomes, important regulators of inflammatory cytokines and effector molecules production (Woods et al., 2017).”
From HDACs and the epigenetic plasticity of cancer cells: target the complexity (2022) · cites this paper as Woods et al., 2017
Hdac11 binds to promoters of Tbet and Eomes.
“Hdac11 binds to promoters and represses transcription of TFs Tbet and Eomes, important regulators of inflammatory cytokines and effector molecules production (Woods et al., 2017).”
From HDACs and the epigenetic plasticity of cancer cells: target the complexity (2022) · cites this paper as Woods et al., 2017
Hdac11 represses transcription of Tbet and Eomes.
“Hdac11 binds to promoters and represses transcription of TFs Tbet and Eomes, important regulators of inflammatory cytokines and effector molecules production (Woods et al., 2017).”
From HDACs and the epigenetic plasticity of cancer cells: target the complexity (2022) · cites this paper as Woods et al., 2017
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- Authors
- Woods, D. M., Woan, K. V., Cheng, F., Sodré, A. L., Wang, D., Wu, Y., Wang, Z., Chen, J., Powers, J., Pinilla-Ibarz, J., Yu, Y., Zhang, Y., Wu, X., Zheng, X., Weber, J., Hancock, W. W., Seto, E., Villagra, A., Yu, X.-Z., & Sotomayor, E. M.
- Affiliations
- Moffitt Cancer Center (US)
- Department of Anatomy and Regenerative Biology, George Washington Cancer Center, Washington, DC;
- University of Pennsylvania (US)
- Department of Medicine and
- Medical University of South Carolina (US)
- Corresponding author
- Woods, David M.
- Woan, Karrune V.
- Yu, Xue-Zhong
- Sotomayor, Eduardo M.
- ORCID
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2017-07-13
- Volume
- 130
- Issue
- 2
- Pages
- 146-155
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- PMC
- PMC5510785
- OpenAlex
- W2619620441
- Cited by
- 74
- References
- 40
- Citations by year
- 2026: 11 · 2025: 2 · 2024: 6 · 2023: 8 · 2022: 9 · 2021: 15 · 2020: 9 · 2019: 7 · 2018: 5 · 2017: 1
- FWCI
- 2.84
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Blood (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Moffitt Cancer Center
- National Cancer Institute (R01CA169116, R01CA179062, R01CA134807, P50CA168536, P30CA076292, P30CA138313)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Histone Deacetylase Inhibitors Research
- Health Sciences › Medicine › Hematology › Hematopoietic Stem Cell Transplantation
- Keywords
- HDAC11, histone deacetylase, T cells, epigenetic regulation, T cell effector function, alloreactivity, graft-versus-host disease, T cell tolerance, interferon-gamma, Eomes, B-cell lymphoma, adoptive T cell therapy, T cell proliferation
- MeSH terms
- T-bet Transcription Factor, Animals, B-Lymphocytes, Chromatin, Disease Models, Animal, Graft vs Host Disease, Interferon-gamma, Lymphocyte Activation, Promoter Regions, Genetic, T-Lymphocytes, Tumor Necrosis Factor-alpha, Signal Transduction, Gene Expression Regulation, Neoplastic, Lymphoma, B-Cell, Mice, Knockout, Adoptive Transfer, T-Box Domain Proteins, Chromatin Immunoprecipitation, Mice, Histone Deacetylase 1
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