Regulation of semaphorin molecules in development of colitis
Project/Area Number |
25860357
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Immunology
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Research Institution | Osaka University |
Principal Investigator |
Kang Sujin 大阪大学, 医学(系)研究科(研究院), 寄附講座助教 (30644398)
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Project Period (FY) |
2013-04-01 – 2016-03-31
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Project Status |
Completed (Fiscal Year 2015)
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Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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Keywords | semaphorin / colitis / セマフォリン / 感染 / 炎症性腸疾患 |
Outline of Final Research Achievements |
Type I Innate lymphoid cells (ILCs) play an important roles in maintenance of intestinal homeostasis. In this study, we identified Sema4A, which is highly expressed in innate lymphoid cells is required for type I ILC activation. Using dextran-sodium induced mouse model, we found that Sema4A deficient mice showed enhanced body weight loss and shortening of colon length from day 5 on. In addition, Sema4A was preferentially expressed in CD8+ T cells in large intestine. Deletion of Sema4A restrained expression of effector molecules such as granzyme B, perfolin and FAS, resulting in susceptible for Listeria sp. infection. Our data demonstrated that Sema4A is essential to prevent excessive intestinal inflammation and for host defense for bacterial infection.
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Report
(4 results)
Research Products
(5 results)
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[Journal Article] mTOR Complex Signaling through the SEMA4A-Plexin B2 Axis Is Required for Optimal Activation and Differentiation of CD8+ T Cells.2015
Author(s)
Ito D, Nojima S*, Nishide M, Okuno T, Takamatsu H, Kang S, Kimura T, Yoshida Y, Morimoto K, Maeda Y, Hosokawa T, Toyofuku T, Ohshima J, Kamimura D, Yamamoto M, Murakami M, Morii E, Rakugi H, Isaka Y, Kumanogoh A*. (* correspondence)
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Journal Title
J Immunol.
Volume: 195
Issue: 3
Pages: 934-943
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research
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