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Conditional Deletion of Histone Deacetylase 1 in T Cells Leads to Enhanced Airway Inflammation and Increased Th2 Cytokine Production

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Zeitschriftentitel: The Journal of Immunology
Personen und Körperschaften: Grausenburger, Reinhard, Bilic, Ivan, Boucheron, Nicole, Zupkovitz, Gordin, El-Housseiny, Lamia, Tschismarov, Roland, Zhang, Yu, Rembold, Martina, Gaisberger, Martin, Hartl, Arnulf, Epstein, Michelle M., Matthias, Patrick, Seiser, Christian, Ellmeier, Wilfried
In: The Journal of Immunology, 185, 2010, 6, S. 3489-3497
Medientyp: E-Article
Sprache: Englisch
veröffentlicht:
The American Association of Immunologists
Schlagwörter:
author_facet Grausenburger, Reinhard
Bilic, Ivan
Boucheron, Nicole
Zupkovitz, Gordin
El-Housseiny, Lamia
Tschismarov, Roland
Zhang, Yu
Rembold, Martina
Gaisberger, Martin
Hartl, Arnulf
Epstein, Michelle M.
Matthias, Patrick
Seiser, Christian
Ellmeier, Wilfried
Grausenburger, Reinhard
Bilic, Ivan
Boucheron, Nicole
Zupkovitz, Gordin
El-Housseiny, Lamia
Tschismarov, Roland
Zhang, Yu
Rembold, Martina
Gaisberger, Martin
Hartl, Arnulf
Epstein, Michelle M.
Matthias, Patrick
Seiser, Christian
Ellmeier, Wilfried
author Grausenburger, Reinhard
Bilic, Ivan
Boucheron, Nicole
Zupkovitz, Gordin
El-Housseiny, Lamia
Tschismarov, Roland
Zhang, Yu
Rembold, Martina
Gaisberger, Martin
Hartl, Arnulf
Epstein, Michelle M.
Matthias, Patrick
Seiser, Christian
Ellmeier, Wilfried
spellingShingle Grausenburger, Reinhard
Bilic, Ivan
Boucheron, Nicole
Zupkovitz, Gordin
El-Housseiny, Lamia
Tschismarov, Roland
Zhang, Yu
Rembold, Martina
Gaisberger, Martin
Hartl, Arnulf
Epstein, Michelle M.
Matthias, Patrick
Seiser, Christian
Ellmeier, Wilfried
The Journal of Immunology
Conditional Deletion of Histone Deacetylase 1 in T Cells Leads to Enhanced Airway Inflammation and Increased Th2 Cytokine Production
Immunology
Immunology and Allergy
author_sort grausenburger, reinhard
spelling Grausenburger, Reinhard Bilic, Ivan Boucheron, Nicole Zupkovitz, Gordin El-Housseiny, Lamia Tschismarov, Roland Zhang, Yu Rembold, Martina Gaisberger, Martin Hartl, Arnulf Epstein, Michelle M. Matthias, Patrick Seiser, Christian Ellmeier, Wilfried 0022-1767 1550-6606 The American Association of Immunologists Immunology Immunology and Allergy http://dx.doi.org/10.4049/jimmunol.0903610 <jats:title>Abstract</jats:title> <jats:p>Chromatin modifications, such as reversible histone acetylation, play a key role in the regulation of T cell development and function. However, the role of individual histone deacetylases (HDACs) in T cells is less well understood. In this article, we show by conditional gene targeting that T cell-specific loss of HDAC1 led to an increased inflammatory response in an in vivo allergic airway inflammation model. Mice with HDAC1-deficient T cells displayed an increase in all critical parameters in this Th2-type asthma model, such as eosinophil recruitment into the lung, mucus hypersecretion, parenchymal lung inflammation, and enhanced airway resistance. This correlated with enhanced Th2 cytokine production in HDAC1-deficient T cells isolated from diseased mice. In vitro-polarized HDAC1-deficient Th2 cells showed a similar enhancement of IL-4 expression, which was evident already at day 3 of Th2 differentiation cultures and restricted to T cell subsets that underwent several rounds of cell divisions. HDAC1 was recruited to the Il4 gene locus in ex vivo isolated nonstimulated CD4+ T cells, indicating a direct control of the Il4 gene locus. Our data provide genetic evidence that HDAC1 is an essential HDAC that controls the magnitude of an inflammatory response by modulating cytokine expression in effector T cells.</jats:p> Conditional Deletion of Histone Deacetylase 1 in T Cells Leads to Enhanced Airway Inflammation and Increased Th2 Cytokine Production The Journal of Immunology
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title Conditional Deletion of Histone Deacetylase 1 in T Cells Leads to Enhanced Airway Inflammation and Increased Th2 Cytokine Production
title_unstemmed Conditional Deletion of Histone Deacetylase 1 in T Cells Leads to Enhanced Airway Inflammation and Increased Th2 Cytokine Production
title_full Conditional Deletion of Histone Deacetylase 1 in T Cells Leads to Enhanced Airway Inflammation and Increased Th2 Cytokine Production
title_fullStr Conditional Deletion of Histone Deacetylase 1 in T Cells Leads to Enhanced Airway Inflammation and Increased Th2 Cytokine Production
title_full_unstemmed Conditional Deletion of Histone Deacetylase 1 in T Cells Leads to Enhanced Airway Inflammation and Increased Th2 Cytokine Production
title_short Conditional Deletion of Histone Deacetylase 1 in T Cells Leads to Enhanced Airway Inflammation and Increased Th2 Cytokine Production
title_sort conditional deletion of histone deacetylase 1 in t cells leads to enhanced airway inflammation and increased th2 cytokine production
topic Immunology
Immunology and Allergy
url http://dx.doi.org/10.4049/jimmunol.0903610
publishDate 2010
physical 3489-3497
description <jats:title>Abstract</jats:title> <jats:p>Chromatin modifications, such as reversible histone acetylation, play a key role in the regulation of T cell development and function. However, the role of individual histone deacetylases (HDACs) in T cells is less well understood. In this article, we show by conditional gene targeting that T cell-specific loss of HDAC1 led to an increased inflammatory response in an in vivo allergic airway inflammation model. Mice with HDAC1-deficient T cells displayed an increase in all critical parameters in this Th2-type asthma model, such as eosinophil recruitment into the lung, mucus hypersecretion, parenchymal lung inflammation, and enhanced airway resistance. This correlated with enhanced Th2 cytokine production in HDAC1-deficient T cells isolated from diseased mice. In vitro-polarized HDAC1-deficient Th2 cells showed a similar enhancement of IL-4 expression, which was evident already at day 3 of Th2 differentiation cultures and restricted to T cell subsets that underwent several rounds of cell divisions. HDAC1 was recruited to the Il4 gene locus in ex vivo isolated nonstimulated CD4+ T cells, indicating a direct control of the Il4 gene locus. Our data provide genetic evidence that HDAC1 is an essential HDAC that controls the magnitude of an inflammatory response by modulating cytokine expression in effector T cells.</jats:p>
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author Grausenburger, Reinhard, Bilic, Ivan, Boucheron, Nicole, Zupkovitz, Gordin, El-Housseiny, Lamia, Tschismarov, Roland, Zhang, Yu, Rembold, Martina, Gaisberger, Martin, Hartl, Arnulf, Epstein, Michelle M., Matthias, Patrick, Seiser, Christian, Ellmeier, Wilfried
author_facet Grausenburger, Reinhard, Bilic, Ivan, Boucheron, Nicole, Zupkovitz, Gordin, El-Housseiny, Lamia, Tschismarov, Roland, Zhang, Yu, Rembold, Martina, Gaisberger, Martin, Hartl, Arnulf, Epstein, Michelle M., Matthias, Patrick, Seiser, Christian, Ellmeier, Wilfried, Grausenburger, Reinhard, Bilic, Ivan, Boucheron, Nicole, Zupkovitz, Gordin, El-Housseiny, Lamia, Tschismarov, Roland, Zhang, Yu, Rembold, Martina, Gaisberger, Martin, Hartl, Arnulf, Epstein, Michelle M., Matthias, Patrick, Seiser, Christian, Ellmeier, Wilfried
author_sort grausenburger, reinhard
container_issue 6
container_start_page 3489
container_title The Journal of Immunology
container_volume 185
description <jats:title>Abstract</jats:title> <jats:p>Chromatin modifications, such as reversible histone acetylation, play a key role in the regulation of T cell development and function. However, the role of individual histone deacetylases (HDACs) in T cells is less well understood. In this article, we show by conditional gene targeting that T cell-specific loss of HDAC1 led to an increased inflammatory response in an in vivo allergic airway inflammation model. Mice with HDAC1-deficient T cells displayed an increase in all critical parameters in this Th2-type asthma model, such as eosinophil recruitment into the lung, mucus hypersecretion, parenchymal lung inflammation, and enhanced airway resistance. This correlated with enhanced Th2 cytokine production in HDAC1-deficient T cells isolated from diseased mice. In vitro-polarized HDAC1-deficient Th2 cells showed a similar enhancement of IL-4 expression, which was evident already at day 3 of Th2 differentiation cultures and restricted to T cell subsets that underwent several rounds of cell divisions. HDAC1 was recruited to the Il4 gene locus in ex vivo isolated nonstimulated CD4+ T cells, indicating a direct control of the Il4 gene locus. Our data provide genetic evidence that HDAC1 is an essential HDAC that controls the magnitude of an inflammatory response by modulating cytokine expression in effector T cells.</jats:p>
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spelling Grausenburger, Reinhard Bilic, Ivan Boucheron, Nicole Zupkovitz, Gordin El-Housseiny, Lamia Tschismarov, Roland Zhang, Yu Rembold, Martina Gaisberger, Martin Hartl, Arnulf Epstein, Michelle M. Matthias, Patrick Seiser, Christian Ellmeier, Wilfried 0022-1767 1550-6606 The American Association of Immunologists Immunology Immunology and Allergy http://dx.doi.org/10.4049/jimmunol.0903610 <jats:title>Abstract</jats:title> <jats:p>Chromatin modifications, such as reversible histone acetylation, play a key role in the regulation of T cell development and function. However, the role of individual histone deacetylases (HDACs) in T cells is less well understood. In this article, we show by conditional gene targeting that T cell-specific loss of HDAC1 led to an increased inflammatory response in an in vivo allergic airway inflammation model. Mice with HDAC1-deficient T cells displayed an increase in all critical parameters in this Th2-type asthma model, such as eosinophil recruitment into the lung, mucus hypersecretion, parenchymal lung inflammation, and enhanced airway resistance. This correlated with enhanced Th2 cytokine production in HDAC1-deficient T cells isolated from diseased mice. In vitro-polarized HDAC1-deficient Th2 cells showed a similar enhancement of IL-4 expression, which was evident already at day 3 of Th2 differentiation cultures and restricted to T cell subsets that underwent several rounds of cell divisions. HDAC1 was recruited to the Il4 gene locus in ex vivo isolated nonstimulated CD4+ T cells, indicating a direct control of the Il4 gene locus. Our data provide genetic evidence that HDAC1 is an essential HDAC that controls the magnitude of an inflammatory response by modulating cytokine expression in effector T cells.</jats:p> Conditional Deletion of Histone Deacetylase 1 in T Cells Leads to Enhanced Airway Inflammation and Increased Th2 Cytokine Production The Journal of Immunology
spellingShingle Grausenburger, Reinhard, Bilic, Ivan, Boucheron, Nicole, Zupkovitz, Gordin, El-Housseiny, Lamia, Tschismarov, Roland, Zhang, Yu, Rembold, Martina, Gaisberger, Martin, Hartl, Arnulf, Epstein, Michelle M., Matthias, Patrick, Seiser, Christian, Ellmeier, Wilfried, The Journal of Immunology, Conditional Deletion of Histone Deacetylase 1 in T Cells Leads to Enhanced Airway Inflammation and Increased Th2 Cytokine Production, Immunology, Immunology and Allergy
title Conditional Deletion of Histone Deacetylase 1 in T Cells Leads to Enhanced Airway Inflammation and Increased Th2 Cytokine Production
title_full Conditional Deletion of Histone Deacetylase 1 in T Cells Leads to Enhanced Airway Inflammation and Increased Th2 Cytokine Production
title_fullStr Conditional Deletion of Histone Deacetylase 1 in T Cells Leads to Enhanced Airway Inflammation and Increased Th2 Cytokine Production
title_full_unstemmed Conditional Deletion of Histone Deacetylase 1 in T Cells Leads to Enhanced Airway Inflammation and Increased Th2 Cytokine Production
title_short Conditional Deletion of Histone Deacetylase 1 in T Cells Leads to Enhanced Airway Inflammation and Increased Th2 Cytokine Production
title_sort conditional deletion of histone deacetylase 1 in t cells leads to enhanced airway inflammation and increased th2 cytokine production
title_unstemmed Conditional Deletion of Histone Deacetylase 1 in T Cells Leads to Enhanced Airway Inflammation and Increased Th2 Cytokine Production
topic Immunology, Immunology and Allergy
url http://dx.doi.org/10.4049/jimmunol.0903610