| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Outline of Final Research Achievements |
I focused on pathophysiology of type1 and type2 autoimmune pancreatitis using this grant. We found mainly three data about autoimmune pancreatitis. Firstly, CD19+CD24highCD38high Bregs seemed to increase reactively to suppress the disease activity. On the other hand, CD19+CD24highCD27+ Bregs might be involved in the development of type 1 AIP, although it still remains unclear whether the decrease of CD19+CD24highCD27+ cells is cause or effect of AIP. Secondly, TLR7 might be a key pattern recognition receptors involved in the development of type 1 AIP including immunosuppressive effect, Th2 type immune response and fibrosis. Third one is that significantly increased neutrophil infiltration around the interlobular pancreatic duct in type2 autoimmune pancreatitis may depend on GCP-2.
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