The analysis of IL-33 inducible Th17 cells in allergic airway inflammation
Project/Area Number |
22790952
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Single-year Grants |
Research Field |
膠原病・アレルギー・感染症内科学
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Research Institution | Tokyo Medical and Dental University |
Principal Investigator |
OHNO Tatsukuni 東京医科歯科大学, 大学院・医歯学総合研究科, 助教 (80435635)
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Project Period (FY) |
2010 – 2011
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Project Status |
Completed (Fiscal Year 2011)
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Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2010: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
Keywords | IL-33 / IL-17 / TH17 / アレルギー性気道炎症 / Th17 / サイトカイン |
Research Abstract |
IL-33 leads to induction of eosinophilic inflammation in the pulmonary mucosa through the IL-4 and IL-13-dependent pathway in mouse asthma model. Taken together, it is thought be that IL-33 may have crucial role in induction of atopic asthma. It is well known that IL-6 induces Th17 cells differentiation. The development of Th17 cells in regional LNs in IL-33 inhaled IL-6 deficient mice is similar to that in wild type mice. These results suggest a novel mechanism for the IL-6 independent Th17 cells differentiation.
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Report
(3 results)
Research Products
(24 results)
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[Journal Article] Th2-, but not Th17-, typeairway inflammation in epicutaneouslyantigen-sensitized mice2012
Author(s)
Morita H, Arae K, Ohno T, Kajiwara N, Oboki K, Matsuda A, Suto H, Okumura K, Sudo K, Takahashi T, Matsumoto K and Nakae S
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Journal Title
Allergol Int
Volume: 61(2)
Pages: 265-73
Related Report
Peer Reviewed
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[Journal Article] ST2 Requires Th2-, but Not Th17-, Type Airway Inflammation in Epicutaneously Antigen- Sensitized Mice2012
Author(s)
Morita H, Arae K, Ohno T, Kajiwara N, Oboki K, Matsuda A, Suto H, Okumura K, Sudo K, Takahashi T, Matsumoto K, Nakae S
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Journal Title
Allergol Int
Volume: (In Press)
NAID
Related Report
Peer Reviewed
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[Journal Article] Paracrine IL-33stimulation enhanceslipopolysaccharide-mediatedmacrophage activation2011
Author(s)
Ohno T, Oboki K, Morita H, Kajiwara N, Arae K, Tanaka S, Ikeda M, Iikura M, Akiyama T, zInoue J, Matsumoto K, SudoK, Azuma M, Okumura K, Kamradt T, Saito H and Nakae S
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Journal Title
PLoSOne
Volume: 11 ; 6(4)
Related Report
Peer Reviewed
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[Journal Article] Okumura K., Kamradt T., Saito H., Nakae S. Paracrine IL-33 stimulation enhances lipopolysaccharide-mediated macrophage2011
Author(s)
Ohno T., Oboki K., Kajiwara N., Tanaka S., Ikeda M., Iikura M., Akiyama T., Inoue J., Matsumoto K., Sudo K., Azuma M.,
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Journal Title
Plos One
Volume: 6
Issue: 4
Pages: 18404-18404
DOI
Related Report
Peer Reviewed
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[Journal Article] IL-33 is a crucialamplifier of innate rather thanacquired immunity2010
Author(s)
Oboki K, Ohno T, Kajiwara N, Arae K, Morita H, Ishii A, Nambu A, Abe T, Kiyonari H, Sudo K, Okumura K, Saito Hand Nakae S
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Journal Title
ProcNatl Acad Sci USA
Volume: 107(43)
Pages: 18581-6
Related Report
Peer Reviewed
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[Journal Article] Development of IL-17-mediateddelayed-type hypersensitivity is notaffected by down-regulation of IL-25expression2010
Author(s)
Ishii A, Oboki K, Nambu A, Morita H, Ohno T, Kajiwara N, Arae K, Sudo H, Okumura K, Saito H, and Nakae S
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Journal Title
Allergol Int
Volume: 59(4)
Pages: 399-408
Related Report
Peer Reviewed
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