| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2011: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2010: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Research Abstract |
We previously demonstrated that Th1 cells gain the capacity to produce IL-13 in response to antigen, IL-2 and IL-18, and based on their unique function, we designated these activated Th1 cells as "super Th1 cells". In this project, we showed that when costimulated with anti-CD3, IL-18 and IL-4, the GATA-binding protein 3(Gata3), which is not originally expressed in Th1 cells, is induced in T-bet-expressing Th1 cells and that Gata3 is essentially required for Il13 gene expression in super Th1 cells. However, Gata3 induction is not satisfactory, and additional TCR-signaling is prerequisite for triggering IL-13 production by Gata3 plus T-bet-expressing Th1 cells. In addition, we revealed that super Th1 cells simultaneously produce IL-22, the amount of which is comparable to that of Th17 cells. Furthermore, we confirmed that when stimulated with anti-CD3, IL-2 and IL-18, Th1 cells strongly increased the expression of Rorc gene, which encodes Rorγt, "Th17-master regulator". These findings suggest that Th1 cells have the capacity to alter their cytokine profile in response to external stimuli.
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