Establishment of novel strategy to treat rheumatoid arthritis by regulating intracellular zinc

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K09521
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Collagenous pathology/Allergology
• Research Institution: Chiba University
• Principal Investigator: Ikeda Kei 千葉大学, 医学部附属病院, 講師 (10456014)
• Co-Investigator(Kenkyū-buntansha): 中島 裕史 千葉大学, 大学院医学研究院, 教授 (00322024) ; 須藤 明 千葉大学, 大学院医学研究院, 准教授 (50447306)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 関節炎 / 亜鉛 / 軟骨 / ヘルパーT細胞

Outline of Final Research Achievements

mRNA expressions of MTF-1 and MMP-3 were increased in the cartilage of ankle in mouse arthritis model (CIA). However, CIA did not exacerbate in cartilage-specific ZIP8 transgenic mice or cartilage-specific MT-1/2 knockout mice. On the other hand, no correlations were identified between mRNA expression of zinc transporters and intracellular zinc concentration in Th17 cells differentiated from mouse naive helper T cells. Furthermore, MT-1/2 knockdown did not affect helper T cell differentiation in vitro.
These data indicate that zinc transporters are not likely to play significant roles in arthritis or helper T cell differentiation in mice.

Free Research Field

リウマチ膠原病学・免疫学