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Antitumor effect after radiofrequency ablation of murine hepatoma is augmented by an active variant of CC chemokine ligand 3/macrophage inflammatory protein-1á

フォーマット:
論文
責任表示:
Iida, Noriho ; Nakamoto, Yasunari ; Baba, Tomohisa ; Nakagawa, Hidetoshi ; Mizukoshi, Eishiro ; Naito, Makoto ; Mukaida, Naofumi ; Kaneko, Shuichi
言語:
英語
出版情報:
American Association for Cancer Research, 2010-08-15
著者名:
Iida, Noriho
Nakamoto, Yasunari
Baba, Tomohisa
Nakagawa, Hidetoshi
Mizukoshi, Eishiro
Naito, Makoto
Mukaida, Naofumi
Kaneko, Shuichi
続きを見る
掲載情報:
Cancer Research
ISSN:
0008-5472  CiNii Articles  Webcat Plus  JAIRO
巻:
70
通号:
16
開始ページ:
6556
終了ページ:
6565
バージョン:
author
概要:
金沢大学医薬保健研究域医学系<br />Several chemokines are used for immunotherapy against cancers because they can attract immune cells such as dendritic and cytotoxic T cells to augment immune responses. Radiofrequency ablation (RFA) is used to loca lly eliminate cancers such as hepatocellular carcinoma (HCC), renal cell carcinoma, and lung cancer. Because HCC often recurs even after an eradicative treatment with RFA, additional immunotherapy is necessary. We treated tumor-bearing mice by administering ECI301, an active variant of CC chemokine ligand 3, after RFA. Mice were injected s.c. with BNL 1ME A.7R.1, a murine hepatoma cell line, in the bilateral flank. After the tumor became palpable, RFA was done on the tumor of one flank with or without ECI301. RFA alone eliminated the treated ipsilateral tumors and retarded the growth of contralateral non-RFA-treated tumors accompanied by massive T-cell infiltration. Injection of ECI301 augmented RFA-induced antitumor effect against non-RFA-treated tumors when administered to wild-type or CCR5-deficient but not CCR1-deficient mice. ECI301 also increased CCR1-expressing CD11c+ cells in peripheral blood and RFA-treated tumors after RFA. Deficiency of CCR1 impairs accumulation of CD11c+, CD4+, and CD8+ cells in RFA-treated tumors. Furthermore, in IFN-ã-enzyme-linked immunospot assay, ECI301 augmented tumor-specific responses after RFA whereas deficiency of CCR1 abolished this augmentation. Thus, we proved that ECI301 further augments RFA-induced antitumor immune responses in a CCR1-dependent manner. ©2010 AACR. 続きを見る
URL:
http://hdl.handle.net/2297/25268

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