Mechanism of allergic inflammation induction of MAP kinase JNK

2019 Fiscal Year Final Research Report

• Project/Area Number: 16K08746
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Experimental pathology
• Research Institution: Tokyo Medical University
• Principal Investigator: Toyota Hiroko 東京医科大学, 医学部, 助手 (80468660)
• Co-Investigator(Kenkyū-buntansha): 矢那瀬 紀子 東京医科大学, 医学部, 講師 (10210303) ; 秦 喜久美 東京医科大学, 医学部, 講師 (30287156) ; 古畑 昌枝 東京医科大学, 医学部, 助手 (90468661)
• Project Period (FY): 2016-04-01 – 2020-03-31
• Keywords: ストレス応答MAPキナーゼJNK

Outline of Final Research Achievements

The nucleoprotein Thy28 molecule has been shown to control antigen receptor-mediated cell death of B and T cells in vitro. We made Thy28TG mice and examined the role of Thy28. Thymic cell death induced by administration of anti-CD3 is suppressed compared to wild-type mice, and suppression of JNK activation and Bcl-xL down-regulation is observed along with suppression of this anti-CD3-induced cell death. It was speculated that Thy28 TG mice were highly sensitive to EAE induced by self-peptides, and the cause thereof was the increase in IFN-g production induced by CD4-positive naive T cells.

Free Research Field

免疫学

Academic Significance and Societal Importance of the Research Achievements

JNK活性化にも関与するThy28がアポトーシス誘導に関わっていることが示唆された。今後さらに実験を重ねThy28機能的役割を明らかにすることによって、アポトーシス誘導機構、さらには癌、自己免疫疾患などの誘導の解明に寄与すると期待できる。