Author
Listed:
- Hiroyuki Hosokawa
(Graduate School of Medicine, Chiba University)
- Tomoaki Tanaka
(Graduate School of Medicine, Chiba University
Graduate School of Medicine, Chiba University
AMED-CREST, AMED)
- Yusuke Endo
(Graduate School of Medicine, Chiba University)
- Miki Kato
(Graduate School of Medicine, Chiba University)
- Kenta Shinoda
(Graduate School of Medicine, Chiba University)
- Akane Suzuki
(Graduate School of Medicine, Chiba University)
- Shinichiro Motohashi
(Graduate School of Medicine, Chiba University)
- Masaki Matsumoto
(Medical Institute of Bioregulation, Kyushu University)
- Keiichi I. Nakayama
(Medical Institute of Bioregulation, Kyushu University)
- Toshinori Nakayama
(Graduate School of Medicine, Chiba University
AMED-CREST, AMED)
Abstract
Th2 cells produce Th2 cytokines such as IL-4, IL-5 and IL-13, but repress Th1 cytokine IFNγ. Recent studies have revealed various distinct memory-type Th2 cell subsets, one of which produces a substantial amount of IFNγ in addition to Th2 cytokines, however it remains unclear precisely how these Th2 cells produce IFNγ. We herein show that phosphorylation of Gata3 at Ser308, Thr315 and Ser316 induces dissociation of a histone deacetylase Hdac2 from the Gata3/Chd4 repressive complex in Th2 cells. We also identify Akt1 as a Gata3-phosphorylating kinase, and the activation of Akt1 induces derepression of Tbx21 and Ifng expression in Th2 cells. Moreover, T-bet-dependent IFNγ expression in IFNγ-producing memory Th2 cells appears to be controlled by the phosphorylation status of Gata3 in human and murine systems. Thus, this study highlights the molecular basis for posttranslational modifications of Gata3 that control the regulation of IFNγ expression in memory Th2 cells.
Suggested Citation
Hiroyuki Hosokawa & Tomoaki Tanaka & Yusuke Endo & Miki Kato & Kenta Shinoda & Akane Suzuki & Shinichiro Motohashi & Masaki Matsumoto & Keiichi I. Nakayama & Toshinori Nakayama, 2016.
"Akt1-mediated Gata3 phosphorylation controls the repression of IFNγ in memory-type Th2 cells,"
Nature Communications, Nature, vol. 7(1), pages 1-12, September.
Handle:
RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms11289
DOI: 10.1038/ncomms11289
Download full text from publisher
Corrections
All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms11289. See general information about how to correct material in RePEc.
If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.
We have no bibliographic references for this item. You can help adding them by using this form .
If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.
For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .
Please note that corrections may take a couple of weeks to filter through
the various RePEc services.