Cytotoxic human peripheral blood-derived γδT cells kill glioblastoma cell lines: implications for cell-based immunotherapy for patients with glioblastoma.

• Material Type: 博士論文
• Title: Cytotoxic human peripheral blood-derived γδT cells kill glioblastoma cell lines: implications for cell-based immunotherapy for patients with glioblastoma.
• Author/Editor: Nakazawa, Tsutomu; Nakamura, Mitsutoshi; Park, Young Soo; Motoyama, Yasushi; Hironaka, Yasuo; Nishimura, Fumihiko; Nakagawa, Ichiro; Yamada, Shuichi; Matsuda, Ryosuke; Tamura, Kentaro; Sugimoto, Tadashi; Takeshima, Yasuhiro; Marutani, Akiko; Tsujimura, Takahiro; Ouji, Noriko; Ouji, Yukiteru; Yoshikawa, Masahide; Nakase, Hiroyuki
• Author Heading: Nakazawa, Tsutomu; Nakamura, Mitsutoshi; Park, Young Soo; Motoyama, Yasushi; Hironaka, Yasuo; Nishimura, Fumihiko; Nakagawa, Ichiro; Yamada, Shuichi; Matsuda, Ryosuke; Tamura, Kentaro; Sugimoto, Tadashi; Takeshima, Yasuhiro; Marutani, Akiko; Tsujimura, Takahiro; Ouji, Noriko; Ouji, Yukiteru; Yoshikawa, Masahide; Nakase, Hiroyuki
• Publication, Distribution, etc.: Springer US
• Publication Date: 2014-01
• Publication Date (W3CDTF): 2014-01
• Alternative Title: ヒト細胞傷害性γδT細胞は膠芽腫細胞株を殺傷する：膠芽腫患者に対する免疫細胞治療の意義
• Periodical title: Journal of neuro-oncology
• No. or year of volume/issue: 116 1
• Volume: 116
• Issue: 1
• Pages: 31-39
• ISSN (Periodical Title): ISSN : 0167-594X
• Degree grantor/type: 奈良県立医科大学
• Date Granted: 2015-05-28
• Dissertation Number: 甲第635号
• Degree Type: 博士（医学）
• Text Language Code: eng
• Subject Heading: γδT cell; Zoledronate; Glioblastoma; Cytotoxicity; Immunotherapy; T-cell receptor
• Target Audience: 一般
• Note (General): type:Thesis; Glioblastoma (GBM) is a highly aggressive brain tumor for which novel therapeutic approaches, such as immunotherapy, are urgently needed. Zoledronate (ZOL), an inhibitor of osteoclastic activity, is known to stimulate peripheral blood-derived γδT cells and sensitize tumors to γδT cell-mediated killing. To investigate the feasibility of γδT cell-based immunotherapy for patients with GBM, we focused on the killing of GBM cell lines by γδT cells and the molecular mechanisms involved in these cell–cell interactions. Peripheral blood mononuclear cells were expanded in ZOL and interleukin (IL)-2 for 14 days, and γδT cells were enriched in the expanded cells by the immunomagnetic depletion of αβT cells. Gliomas are resistant to NK cells but susceptible to lymphokine-activated killer cells and some cytotoxic T lymphocytes. When the γδT cell-mediated killing of three GBM cell lines (U87MG, U138MG and A172 cells) and an NK-sensitive leukemia cell line (K562 cells) were tested, 32 % U87MG, 15 % U138MG, 1 % A172, and 50 % K562 cells were killed at an effector:target ratio of 5:1. The γδT cell-mediated killing of all three GBM cell lines was significantly enhanced by ZOL and this ZOL-enhanced killing was blocked by an anti-T cell receptor (TcR) antibody. These results indicated that TcR γδ is crucial for the recognition of ZOL-treated GBM cells by γδT cells. Since the low level killing of GBM cells by the γδT cells was enhanced by ZOL, γδT cell-targeting therapy in combination with ZOL treatment could be effective for patients with GBM.; 博士（医学）・甲第635号・平成27年5月28日; © Springer Verlag. The definitive version is available at " http://dx.doi.org/10.1007/s11060-013-1258-4 "; identifier:Journal of neuro-oncology Vol.116 No.1 p.31-39(2014.01); identifier:0167594X; identifier:http://ginmu.naramed-u.ac.jp/dspace/handle/10564/3068; identifier:Journal of neuro-oncology, 116(1): 31-39
• Source: fulltext; http://ginmu.naramed-u.ac.jp/dspace/bitstream/10564/3068/1/01_%e7%94%b2635%e6%9c%ac%e6%96%87%e3%81%ae%e8%a6%81%e6%97%a8.pdf; http://ginmu.naramed-u.ac.jp/dspace/bitstream/10564/3068/2/02_%e7%94%b2635%e5%af%a9%e6%9f%bb%e8%a6%81%e6%97%a8.pdf; http://ginmu.naramed-u.ac.jp/dspace/bitstream/10564/3068/3/03_%e7%94%b2635%e6%9c%ac%e6%96%87.pdf
• Access Restrictions: インターネット公開
• Related Material (DOI): 10.1007/s11060-013-1258-4
• Periodical Title (NCID): AA10633712; https://ci.nii.ac.jp/ncid/AA10633712
• Data Provider (Database): 国立情報学研究所 : 学術機関リポジトリデータベース（IRDB）（機関リポジトリ）; https://irdb.nii.ac.jp
• Original Data Provider (Database): 奈良県立医科大学 : 奈良県立医科大学機関リポジトリ GINMU