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.