The histone deacetylase inhibitor Trichostatin A modulates CD4+ T cell responses

José Manuel Alfonso Moreira; Peter Scheipers; Poul Sørensen

doi:10.1186/1471-2407-3-30

The histone deacetylase inhibitor Trichostatin A modulates CD4+ T cell responses

José Manuel Alfonso Moreira, Peter Scheipers, Poul Sørensen

119 Citations (Scopus)

Abstract

Histone deacetylase inhibitors (HDACIs) induce hyperacetylation of core histones modulating chromatin structure and affecting gene expression. These compounds are also able to induce growth arrest, cell differentiation, and apoptotic cell death of tumor cells in vitro as well as in vivo. Even though several genes modulated by HDAC inhibition have been identified, those genes clearly responsible for the biological effects of these drugs have remained elusive. We investigated the pharmacological effect of the HDACI and potential anti-cancer agent Trichostatin A (TSA) on primary T cells.

Original language	English
Journal	B M C Cancer
Volume	3
Pages (from-to)	30
ISSN	1471-2407
DOIs	https://doi.org/10.1186/1471-2407-3-30
Publication status	Published - 2003

Keywords

Animals
Antigens, CD
Apoptosis
CD4-Positive T-Lymphocytes
Caspases
Enzyme Inhibitors
Female
Gene Expression Regulation
Histone Deacetylase Inhibitors
Hydroxamic Acids
Interleukin-2
Lymphocyte Activation
Mice
Mice, Inbred C57BL
NF-kappa B
Reactive Oxygen Species
Signal Transduction
Transcriptional Activation

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1186/1471-2407-3-30

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title = "The histone deacetylase inhibitor Trichostatin A modulates CD4+ T cell responses",

abstract = "Histone deacetylase inhibitors (HDACIs) induce hyperacetylation of core histones modulating chromatin structure and affecting gene expression. These compounds are also able to induce growth arrest, cell differentiation, and apoptotic cell death of tumor cells in vitro as well as in vivo. Even though several genes modulated by HDAC inhibition have been identified, those genes clearly responsible for the biological effects of these drugs have remained elusive. We investigated the pharmacological effect of the HDACI and potential anti-cancer agent Trichostatin A (TSA) on primary T cells.",

keywords = "Animals, Antigens, CD, Apoptosis, CD4-Positive T-Lymphocytes, Caspases, Enzyme Inhibitors, Female, Gene Expression Regulation, Histone Deacetylase Inhibitors, Hydroxamic Acids, Interleukin-2, Lymphocyte Activation, Mice, Mice, Inbred C57BL, NF-kappa B, Reactive Oxygen Species, Signal Transduction, Transcriptional Activation",

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year = "2003",

doi = "10.1186/1471-2407-3-30",

language = "English",

volume = "3",

pages = "30",

journal = "B M C Cancer",

issn = "1471-2407",

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TY - JOUR

T1 - The histone deacetylase inhibitor Trichostatin A modulates CD4+ T cell responses

AU - Moreira, José Manuel Alfonso

AU - Scheipers, Peter

AU - Sørensen, Poul

PY - 2003

Y1 - 2003

N2 - Histone deacetylase inhibitors (HDACIs) induce hyperacetylation of core histones modulating chromatin structure and affecting gene expression. These compounds are also able to induce growth arrest, cell differentiation, and apoptotic cell death of tumor cells in vitro as well as in vivo. Even though several genes modulated by HDAC inhibition have been identified, those genes clearly responsible for the biological effects of these drugs have remained elusive. We investigated the pharmacological effect of the HDACI and potential anti-cancer agent Trichostatin A (TSA) on primary T cells.

AB - Histone deacetylase inhibitors (HDACIs) induce hyperacetylation of core histones modulating chromatin structure and affecting gene expression. These compounds are also able to induce growth arrest, cell differentiation, and apoptotic cell death of tumor cells in vitro as well as in vivo. Even though several genes modulated by HDAC inhibition have been identified, those genes clearly responsible for the biological effects of these drugs have remained elusive. We investigated the pharmacological effect of the HDACI and potential anti-cancer agent Trichostatin A (TSA) on primary T cells.

KW - Animals

KW - Antigens, CD

KW - Apoptosis

KW - CD4-Positive T-Lymphocytes

KW - Caspases

KW - Enzyme Inhibitors

KW - Female

KW - Gene Expression Regulation

KW - Histone Deacetylase Inhibitors

KW - Hydroxamic Acids

KW - Interleukin-2

KW - Lymphocyte Activation

KW - Mice

KW - Mice, Inbred C57BL

KW - NF-kappa B

KW - Reactive Oxygen Species

KW - Signal Transduction

KW - Transcriptional Activation

U2 - 10.1186/1471-2407-3-30

DO - 10.1186/1471-2407-3-30

M3 - Journal article

C2 - 14606959

SN - 1471-2407

VL - 3

SP - 30

JO - B M C Cancer

JF - B M C Cancer

ER -

The histone deacetylase inhibitor Trichostatin A modulates CD4+ T cell responses

Abstract

Keywords

UN SDGs

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