Akt1-mediated Gata3 phosphorylation controls the repression of IFNγ in memory-type Th2 cells

Hiroyuki Hosokawa, Tomoaki Tanaka, Yusuke Endo, Miki Kato, Kenta Shinoda, Akane Suzuki, Shinichiro Motohashi, Masaki Matsumoto, Keiichi I. Nakayama and Toshinori Nakayama ()
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Hiroyuki Hosokawa: Graduate School of Medicine, Chiba University
Tomoaki Tanaka: Graduate School of Medicine, Chiba University
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

Nature Communications, 2016, vol. 7, issue 1, 1-12

Abstract: 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.

Date: 2016
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms11289

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DOI: 10.1038/ncomms11289

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