| Project/Area Number |
23591017
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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 |
Gastroenterology
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| Research Institution | Kansai Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
NISHIO Akiyoshi 関西医科大学, 医学部, 准教授 (50362463)
UCHIDA Kazushige 関西医科大学, 医学部, 講師 (40411516)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2011: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | IgG4関連疾患 / 自己免疫性膵炎 / IgG4 / 制御性T細胞 / 制御性B細胞 / 自然免疫 / ＩｇＧ４ / 制御性Ｔ細胞 / 制御性Ｂ細胞 |
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| Research Abstract |
(1)In pancreas cancer and obstructive pancreatitis type 1 AIP, infiltration of memory regulatory T cells (Tregs) and IgG4-positive cells were positively correlated, which suggested that increased memory-Tregs may be an inhibitory immune response against inflammation, although decreased naïve Tregs may be pathogenic. (2) We identified two subtypes of regulatory B cells (Bregs), CD19+CD24highCD38high Bregs and CD19+CD24highCD27+ Bregs in type 1 AIP. The increased CD19+CD24highCD38high Bregs may suppress the disease activity of type 1 AIP, whereas the decreased CD19+CD24highCD27+ Bregs might be involved in the development of type 1 AIP. (3) In animal models, activation of TLR3 (polyinosinic:polycytidylic acid) can induce immune-mediated cholangitis, pancreatitis and sialadenitis similar to human autoimmune pancreatitis.
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