| Project/Area Number |
25670213
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Bacteriology (including mycology)
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| Research Institution | Kyushu University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | NOTCH / Bcl11b / IL-7R / IL-17A / IFN-γ / γδT細胞 / CD30L / CD30 / 細菌学 / T細胞 / 免疫学 / γδ細胞 / 細菌感染 |
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| Outline of Final Research Achievements |
Early T cell precursors at the double-negative (DN) 2 or 3 stages in fetal thymus are committed to IL-17A or IFN-γ γδ T cells.We found that IL-17A γδ T cells developed directly from DN2b cells in Notch/Hes1, Notch/Bcl11b and Notch/IL-7Rα-dependent pathways, whereas two types of IFN-γ γδ T cells developed from DN2a or DN3 stage in fetal thymus, respectively. CD30 and CD30L were selectively expressed by IL-17A γδ T cells and the number was drastically reduced in CD30L or CD30 knock out mice. In vivo administration of soluble CD30 protein (CD30-Ig) impaired the early protection against Listeria monocytogenes or Mycobacterium bovis Bacillus Calmette-Guerin infection,while agonistic anti-CD30 monoclonal antibody enhanced the protection by activating the IL-17A γδ T cells. CD30L/CD30 signaling plays an important role in the activation of IL-17A γδ T cells at the early stage for protection against bacterial infection.
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