Open AccessCutting Edge: Negative Regulation of Dendritic Cells through Acetylation of the Nonhistone Protein STAT-3
Author(s) -
Yaping Sun,
Y. Eugene Chin,
Elizabeth Weisiger,
Chelsea Malter,
Isao Tawara,
Tomomi Toubai,
Erin Gatza,
Paolo Mascagni,
Charles A. Dinarello,
Pavan Reddy
Publication year - 2009
Publication title -
the journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.737
H-Index - 372
eISSN - 1550-6606
pISSN - 0022-1767
DOI - 10.4049/jimmunol.0804388
Subject(s) - acetylation , stat , hdac1 , histone deacetylase , microbiology and biotechnology , immune system , histone , transcription factor , dendritic cell , transcription (linguistics) , chemistry , biology , signal transduction , immunology , stat3 , biochemistry , gene , linguistics , philosophy
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.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom