| Budget Amount *help |
¥14,400,000 (Direct Cost: ¥14,400,000)
Fiscal Year 2005: ¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 2004: ¥11,700,000 (Direct Cost: ¥11,700,000)
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| Research Abstract |
Autoimmune pancreatitis is a unique form of chronic pancreatitis characterized by swelling of the pancreatic parenchyma, irregular narrowing of the main pancreatic duct, obstructive jaundice, high serum IgG concentration, lymphoplasmacytic infiltration in the pancreatic tissue and favorable response to corticosteroid therapy. We previously revealed that this disease is significantly associated with high serum IgG4 concentration and HLA DRB1^*0405-DQB1^*0401 haplotype. However, pathogenesis has not been fully elucidated. The aim of the present study was to clarify whether mannose binding pathway of complement activation system is operating in the pathogenesis, and to survey genome wide analysis of autioimmune pancreatitis associated genes using microsatellite markers covering entire chromosome. The results showed that autoimmune pancreatitis exhibits a high serum circulating immune complex values in its active stage, which links to a complement activation system with a classical pathway, rather than the mannose-binding lectin pathway or alternative pathway. We found 18 associated microsatellite markers, 12 sensitive and 6 resistant, which exist in chromosome 1, 4, 5, 6, 9, 10, 12, 13, 15, 18 and X. Near the these markers, we identified some candidate disease associated genes. In conclusion, we clarified that autoimmune pancreatitis is closely associated with classical pathway of complement activation system in its active stage, and identified some candidate disease associated genens.
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