Regulation of Immune Responses by the transcription regulatior IkappaBzeta and its binding protein

2018 Fiscal Year Final Research Report

• Project/Area Number: 16K08747
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Experimental pathology
• Research Institution: Toho University
• Principal Investigator: YAMAZAKI Soh 東邦大学, 医学部, 准教授 (70315084)
• Research Collaborator: KATAGIRI Takaharu
• Project Period (FY): 2016-04-01 – 2019-03-31
• Keywords: IkappaBzeta / JunB / Th17 / 自己免疫疾患

Outline of Final Research Achievements

Although IL-17-producing T helper (Th17) cells are associated with autoimmune diseases such as multiple sclerosis, development of the cells has not been fully understood. While the transcription factor JunB is known to be involved in barrier function of skin and regulation of myeloid cells, it role in immune cells was not known. We elucidated that Junb-deficient naive CD4+ T cells were incapable of differentiating into Th17 cells, and that mice deficient in JunB are totally resistant to EAE, an animal model for human multiple sclerosis.

Free Research Field

免疫学　生化学

Academic Significance and Societal Importance of the Research Achievements

多発性硬化症をはじめ、リウマチ関節炎や乾癬などの自己免疫疾患は治療戦略はもとより、病態の発症メカニズムについても詳細が不明だった。今回の発見に基づき、JunBのはたらきを阻害するというアプローチにより自己免疫疾患を抑えるという新しい治療法の可能性が開けた。