2010 Fiscal Year Final Research Report
The elucidation of host defense mechanisms of Mycobacterium tuberculosis infection and the architecture of cytokine-network.
| 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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| Keywords | 感染免疫 |
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| 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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