| Project/Area Number |
20590449
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Bacteriology (including Mycology)
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| Research Institution | University of the Ryukyus |
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Principal Investigator |
UMEMURA Masayuki University of the Ryukyus, 熱帯生物圏研究センター, 助教 (90359985)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUZAKI Goro 琉球大学, 熱帯生物圏研究センター, 教授 (30229455)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2010: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2009: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2008: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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|---|
| Keywords | 感染免疫 / 結核菌 / 肺感染 / サイトカイン / IL-17 / 感染防御 / 細胞内寄生性細菌 / インターロイキン-17 / 自然免疫 / 獲得免疫 / 肉芽腫形成 |
|---|
| Research Abstract |
IL-17A is a proinflammatory cytokine that enhances generation, activation,and migration of neutrophils. Recently, IL-17A has been reported to provide protections against various pathogens, including mycobacteria species. We have previously reported that IL-17 involves in the immune response against mycobacterial infection through neutrophil recruitment and enhancement of Th1 response. Although IL-17A is generally considered as Th17 cell product, we identified that TCR γδ T cells are the major IL-17A-producing cells in vivo. Furthermore, the lack of IL-17A resulted in reduced IFN-γ production by mycobacteria-specific CD4^+ T cells and impaired granuloma formation after mycobacterial infection. Our data suggest that IL-17A is an important inducer of optimal Th1 response and protective immunity against mycobacterial infection.
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