Challenge to establish new preventive and therapeutic methods for rheumatoid arthritis

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K09522
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Collagenous pathology/Allergology
• Research Institution: University of Toyama
• Principal Investigator: Tatsuhiko Ozawa 富山大学, 大学院医学薬学研究部(医学), 助教 (10432105)
• Co-Investigator(Renkei-kenkyūsha): KATO Ryuichi 大学共同利用機関法人高エネルギー加速器研究機構, 物質構造科学研究所, 准教授 (50240833)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: モノクローナルACPA / 関節リウマチ / シトルリン化 / ISAAC法 / フィブリノーゲン

Outline of Final Research Achievements

We tried to identify for nondenaturing proteins recognized by CCP-Ab1, an autoantibody derived from rheumatoid arthritis patients. Our findings demonstrated that a monoclonal ACPA (CCP-Ab1) bound to fibrinogen under native conditions. Next, we made the amino acid sequences of CCP-Ab1 revert to their germline sequences (CCP-Ab1 GL-rev) and analyzed its binding activity to the fibrinogen. CCP-Ab1 GL-rev did not bound to fibrinogen. These results suggested that CCP-Ab1 was generated by the stimulation of B-cells with citrullinated denatured protein and it acquired the reactivity to fibrinogen during B-cell differentiation by somatic hypermutation.

Free Research Field

抗体工学