Cutting edge: Negative regulation of dendritic cells through acetylation of the nonhistone protein STAT-3
Y Sun, YE Chin, E Weisiger, C Malter… - The Journal of …, 2009 - journals.aai.org
Y Sun, YE Chin, E Weisiger, C Malter, I Tawara, T Toubai, E Gatza, P Mascagni…
The Journal of Immunology, 2009•journals.aai.orgHistone deacetylase (HDAC) inhibition modulates dendritic cell (DC) functions and
regulates experimental graft-vs-host disease and other immune-mediated diseases. The
mechanisms by which HDAC inhibition modulates immune responses remain largely
unknown. STAT-3 is a transcription factor shown to negatively regulate DC functions. In this
study we report that HDAC inhibition acetylates and activates STAT-3, which regulates DCs
by promoting the transcription of IDO. These findings demonstrate a novel functional role for …
regulates experimental graft-vs-host disease and other immune-mediated diseases. The
mechanisms by which HDAC inhibition modulates immune responses remain largely
unknown. STAT-3 is a transcription factor shown to negatively regulate DC functions. In this
study we report that HDAC inhibition acetylates and activates STAT-3, which regulates DCs
by promoting the transcription of IDO. These findings demonstrate a novel functional role for …
Abstract
Histone deacetylase (HDAC) inhibition modulates dendritic cell (DC) functions and regulates experimental graft-vs-host disease and other immune-mediated diseases. The mechanisms by which HDAC inhibition modulates immune responses remain largely unknown. STAT-3 is a transcription factor shown to negatively regulate DC functions. In this study we report that HDAC inhibition acetylates and activates STAT-3, which regulates DCs by promoting the transcription of IDO. These findings demonstrate a novel functional role for posttranslational modification of STAT-3 through acetylation and provide mechanistic insights into HDAC inhibition-mediated immunoregulation by induction of IDO.
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