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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| 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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Report
(4 results)
Research Products
(85 results)
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[Journal Article] Essential role of interleukin-17A in the formation of a mycobacterial infection-induced granuloma in the lung.2010
Author(s)
Okamoto, Y., Umemura, M., Yahagi, A., O'Brien, R.L., Ikuta, K., Kishihara, K., Hara, H., Nakae, S., Iwakura, Y., Matsuzaki, G.
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Journal Title
The Journal of Immunology
Volume: 184
Pages: 4414-4422
Related Report
Peer Reviewed
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[Journal Article] Suppressed induction of mycobacterial antigen-specific Th1-type CD4+ T cells in the lung after pulmonary mycobacterial infection.2010
Author(s)
Yahagi, A., Umemura, M., Tamura, T., Kariyone, A., Begum, M.D., Kawakami, K., Okamoto, Y., Oshiro, K., Kohama, H., Arakawa, T., Ohara, N., Takatsu, K., Matsuzaki, G.
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Journal Title
International Immunology
Volume: 22
Pages: 307-318
Related Report
Peer Reviewed
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[Journal Article]2010
Author(s)
梅村正幸
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Journal Title
Medical Science Digest, IL-17産生性T細胞と疾患「細菌感染防御におけるIL-17産生性T細胞の役割」(ニュー・サイエンス社)
Pages: 25-28
Related Report
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