Can the cell surface marker detected by our new culture system be a therapeutic target for inflammatory bowel disease (IBD)?

• Project/Area Number: 15K21179
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Gastroenterology; Immunology
• Research Institution: Okayama University
• Principal Investigator: Takahara Masahiro 岡山大学, 医学部, 客員研究員 (80738427)
• Research Collaborator: Takaki Akinobu ; Hiraoka Sakiko
• Project Period (FY): 2015-04-01 – 2018-03-31
• Project Status: Completed (Fiscal Year 2017)
• Budget Amount: ¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000); Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000); Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000); Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
• Keywords: CD25 / CD4+T細胞 / 制御性T細胞 / 炎症性腸疾患 / CD4 + T細胞

Outline of Final Research Achievements

We investigated whether CD25, which was detected by our new culture system, could be a therapeutic target on inflammatory bowel disease. The lamina propria (LP) CD4+ T cells of colitis mice were cultured under standard mitogen stimulation and collected. The collected LPCD4+T cells were compared to the inflammatory cytokines productions by flow cytometric analysis. Additionally, we sorted CD25 positive and negative cells from LPCD4+ T cells of colitis mice and transferred each fractions separately into new immunodeficiency mice and compared the severity of colitis.
As the CD25 positive cells contain CD4+CD25+Foxp3+ regulatory T cells (Treg cells), we excluded the Treg cells fraction and compared the inflammatory cytokines production with the CD25 negative cells. The cytokines production was not different between the Treg negative CD25 positive cells and the CD25 negative cells fraction.We are now investigating the in vivo experiments.