Development of the molecular target therapy for the inflammatory bowel disease
| Project/Area Number |
16H05169
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Experimental pathology
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| Research Institution | University of Tsukuba |
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Principal Investigator |
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| Research Collaborator |
Sato Kazuki
Kanemaru Yumi (Yamashita Yumi)
Abe Fumie
Nakamura Yuho
Murata Rikito
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥17,550,000 (Direct Cost: ¥13,500,000、Indirect Cost: ¥4,050,000)
Fiscal Year 2018: ¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥5,720,000 (Direct Cost: ¥4,400,000、Indirect Cost: ¥1,320,000)
Fiscal Year 2016: ¥6,890,000 (Direct Cost: ¥5,300,000、Indirect Cost: ¥1,590,000)
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| Keywords | 免疫学 / 免疫受容体 / 制御性T細胞 / 炎症 / 免疫系受容体 / 炎症性腸炎 / 炎症性腸疾患 |
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| Outline of Final Research Achievements |
The inflammatory bowel disease is an intractable disease with chronic inflammation of the intestinal mucosa. Treg cells play an important role to suppress immune response-induced inflammation. Here, we found that DNAM-1 induced instability of Foxp3 expression, which is a master regulator for Treg cells, under the inflammation. Moreover, we observed that the treatment with an anti-DNAM-1 neutralizing antibody ameliorated inflammation via upregulation of Treg stability. These results suggested that DNAM-1 might be a useful target for the therapy of the inflammatory bowel disease.
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| Academic Significance and Societal Importance of the Research Achievements |
クローン病や潰瘍性大腸炎に代表される炎症性腸疾患は、腸粘膜の慢性炎症を主徴とする原因不明の難治性疾患である。わが国の患者数は年々増加おり、H25年には20万人を超えた（難病情報センター発表）。しかし、根治的治療法が未だ確立されていないことより、早急な治療法の開発が望まれている。本研究にて炎症性疾患モデル動物に抗DNAM-1中和抗体を投与するとTregの免疫抑制能が上昇し、病態を軽減したことから、DNAM-1が有用な治療標的となる可能性が示唆された。
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Report
(4 results)
Research Products
(52 results)
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[Journal Article] Soluble DNAM-1, as a predictive biomarker for acute graft-versus-host disease.2016
Author(s)
Kanaya M, Shibuya K, Hirochika R, Kanemoto M, Ohashi K, Okada M, Wagatsuma Y, Cho Y, Kojima H, Teshima T, Imamura M, Sakamaki H, Shibuya A.
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Journal Title
DOI
NAID
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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[Journal Article] Marginal zone B cells exacerbate endotoxic shock via interleukin-6 secretion induced by Fcα/μR-coupled TLR4 signalling. , :, 20162016
Author(s)
Honda S, Sato K, Totsuka N, Fujiyama S, Fujimoto M, Miyake K, Nakahashi-Oda C, Tahara-Hanaoka S, Shibuya K, Shibuya A
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Journal Title
Nature Communications,
Volume: 7
Pages: 1-10
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research / Acknowledgement Compliant
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[Journal Article] Increased Soluble CD155 in the Serum of Cancer Patients2016
Author(s)
Iguchi-Manaka A, Okumura G, Kojima H, Cho Y, Hirochika R, Bando H, Sato T, Yoshikawa H, Hara H, Shibuya A, Shibuya K.
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Journal Title
PLoS ONE
Volume: 11(4)
Pages: 1-12
DOI
NAID
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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[Presentation] Apoptotic epithelial cells control the abundance of regulatory T cells at barrier surfaces.2016
Author(s)
Nakahashi-Oda C, Udayanga K. G. S, Nakamura Y, Nakazawa Y, Totsuka N, Miki H, Iino S, Tahara-Hanaoka S, Honda S, Shibuya K, Shibuya A.
Organizer
International Congress of Immunology 2016
Place of Presentation
Melbourne (Australia)
Year and Date
2016-08-22
Related Report
Int'l Joint Research
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