| Project/Area Number |
26460568
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Immunology
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| Research Institution | Yamagata University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
奈良 英利 山形大学, 医学部, 助教 (00375338)
武田 裕司 山形大学, 医学部, 助教 (90302299)
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| Co-Investigator(Renkei-kenkyūsha) |
ASAO NAOKI 東北大学, 理学系研究科, 教授 (60241519)
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| Research Collaborator |
ARAKI AKEMI 山形大学, 医学部, 技術専門職員
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 炎症性発がん / サイトカイン / インターロイキン21 / AID / 炎症性発癌 / IL-21 / 炎症性腸疾患 |
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| Outline of Final Research Achievements |
Chronic inflammation is a strong background factor of carcinogenesis. When colitis-associated colorectal cancer (CAC) was induced in our Tg mice expressing IL-21 isoform specifically in T cells, the incidence of cancer increased. IL-21 enhances AID expression on B cells and induces antibody class switching and somatic hyper mutations. Therefore, the possibility that the induction of AID by IL-21 may be involved in the development of CAC was investigated.
AID expression tended to increase in CAC-induced Tg colon epithelial cells (IEC) than in wild type mice, and IL-21 directly enhanced AID expression in isolated IEC. These results suggested that IL-21 may enhance the expression of AID in inflamed IEC and may induce CAC.
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