Examination of factors disturbed ADCC activity of NK cells to the solid tumor

• Project/Area Number: 17K10613
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Digestive surgery
• Research Institution: Kawasaki Medical School
• Principal Investigator: TOMIO UENO 川崎医科大学, 医学部, 教授 (70284255)
• Co-Investigator(Kenkyū-buntansha): 吉村 清 国立研究開発法人国立がん研究センター, 中央病院, 医長 (30346564)
• Project Period (FY): 2017-04-01 – 2020-03-31
• Project Status: Completed (Fiscal Year 2019)
• Budget Amount: ¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000); Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000); Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000); Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
• Keywords: ADCC / NK細胞 / HER２ / 胃癌 / ADCC活性 / 免疫療法 / 胃がん / 抗体依存性細胞障害 / 抗Her2抗体 / 人工知能

Outline of Final Research Achievements

The aim of this study is to examine the factors which disturbed the activity of antibody-dependent cell-mediated cytotoxicity (ADCC) of natural killer T cells (NK cells) to the solid tumor and to improve the effect of antibody dependent immunotherapy. We co-incubated NK cells with either HER2+ human gastric cancer cell line (HSC-60) or HER2+ human breast cancer cell line (SK-BR-3), while adding anti-HER2 antibody. Also, we co-incubated NK cells with HER2- human breast cancer cell line (HCC1599), adding anti-HER2 antibody. We observed each ADCC activity of NK cells. We investigated the surface marker which appeared on alive cells after treatment. As a result, cells which have HER2 protein at the surface, could impair ADCC activity of NK cells.

Academic Significance and Societal Importance of the Research Achievements

固形がんに対するNK細胞浸潤能向上のための、基礎データとなる。