2011 Fiscal Year Final Research Report
The expression of"non-Th1"cytokines by"super Th1 cells"
| Project/Area Number |
22790476
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Immunology
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| Research Institution | Hyogo Medical University |
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Principal Investigator |
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| Project Period (FY) |
2010 – 2011
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| Keywords | 免疫学 / アレルギー・ぜんそく / シグナル伝達 / 発現制御 |
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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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[Journal Article] Contribution of IL-18 to eosinophilic airway inflammation induced by immunization and challenge with Staphylococcus aureus proteins2010
Author(s)
Kuroda-Morimoto M, Tanaka H, Hayashi N, Nakahira M, Imai Y, Imamura M, Yasuda K, Yumikura-Futatsugi S, Matsui K, Nakashima T, Sugimura K, Tsutsui H, Sano H, Nakanishi K.
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Journal Title
Int Immunol.
Volume: Vol.22 No.7
Pages: 561-70
DOI
Peer Reviewed
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