Study of the pathogenesis of autoimmune pancreatitis and, the relation to activation of immate immunity induced by bacteria

2015 Fiscal Year Final Research Report

• Project/Area Number: 23590522
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Bacteriology (including Mycology)
• Research Institution: Tokyo Women's Medical University
• Principal Investigator: HARUTA Ikuko 東京女子医科大学, 医学部, 准教授 (80221513)
• Co-Investigator(Kenkyū-buntansha): YAGI Junji 東京女子医科大学, 医学部, 教授 (70182300)
• Project Period (FY): 2011-04-28 – 2016-03-31
• Keywords: 自己免疫性膵炎 / IgG4関連疾患 / 自然免疫 / FliC / 自己免疫疾患 / 制御性T細胞

Outline of Final Research Achievements

We previously established a mouse model of AIP using chronic exposure to a commensal bacteria, Escherichia coli, leading to pancreatic inflammation, and elevation in IgG and IgG1 in serum and detection of anti-lactoferrin and anticarbonic anhydrace-II. The outer membrane fractions of E. coli were subjected to two-dimensional gel electrophoresis followed by immunoblotting against sera from the AIP model. One representative immunoreactive spot was determined using TOF/MS and Mascot search as FliC. Sera from patients with AIP had a signiticcantly higher antibody titer. Therefore, we are underway to clarify the possibility of a new diagnostic value of anti FliC-Ab titer.

Free Research Field

免疫学、消化器内科学