Molecular basis and therapeutic target for autoimmune arthritis

2016 Fiscal Year Final Research Report

• Project/Area Number: 26253030
• Research Category: Grant-in-Aid for Scientific Research (A)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Immunology
• Research Institution: Osaka University
• Principal Investigator: Sakaguchi Shimon 大阪大学, 免疫学フロンティア研究センター, 教授 (30280770)
• Co-Investigator(Kenkyū-buntansha): 廣田 圭司 京都大学, 再生医科学研究所, 准教授 (90631250)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: SKG / 自己免疫性関節炎 / 関節リウマチ

Outline of Final Research Achievements

In this study, we have developed a new mouse model system with different ZAP-70 functions to understand the development and autoimmune function of T helper cells and identified a particular range of ZAP-70 function associated with the developmental arrest of T cells in the thymus and generation of arthritogenic T helper cells. We have also established a novel retrogenic mouse system to identify auto-antigens recognized by arthritogenic T cells isolated from inflamed joints of SKG mice and demonstrated that T cells specific for the auto-antigen RPL23A induced psoriasis-like skin disease and arthritis. Anti-RPL23A auto-antibody was specific to patients with rheumatoid arthritis, indicating that this screening system for auto-antigens is useful for identifying novel therapeutic targets and new biomarkers for rheumatoid arthritis.

Free Research Field

免疫学