Regulation of GM-CSF-producing Th cells

2016 Fiscal Year Final Research Report

• Project/Area Number: 26670477
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Collagenous pathology/Allergology
• Research Institution: Kyoto University (2015-2016); Osaka University (2014)
• Principal Investigator: Hirota Keiji 京都大学, ウイルス・再生医科学研究所, 准教授 (90631250)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: サイトカイン / ヘルパーT細胞 / GM-CSF

Outline of Final Research Achievements

In this study, we identified TNFRSF18 as a specific surface molecule for the regulation of GM-CSF by activated Th cells in vitro. The activation of TNFRSF18 signaling also induced GM-CSF production from effector/memory Th cells in vivo, indicating that this signal cascade is a key molecular pathway to specifically enhance production of GM-CSF. Furthermore, TNFSF18-deficient mice were resistant to the development of experimental autoimmune encephalomyelitis, accompanying impaired production of GM-CSF by tissue infiltrating pathogenic Th cells. Thus, targeting this molecular pathway may be useful for a therapeutic means to prevent or treat the autoimmune disease.

Free Research Field

免疫学