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Tumor cell apoptosis induces tumor-specific immunity in a CC chemokine receptor 1- and 5-dependent manner in mice
https://doi.org/10.24517/00027539
https://doi.org/10.24517/000275391cc96838-1cac-4e5d-9ceb-d8cd16de5a03
| 名前 / ファイル | ライセンス | アクション |
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CA-PR-MUKAIDA-N-1001.pdf (1.2 MB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||||||||||
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| 公開日 | 2017-11-09 | |||||||||||||
| タイトル | ||||||||||||||
| タイトル | Tumor cell apoptosis induces tumor-specific immunity in a CC chemokine receptor 1- and 5-dependent manner in mice | |||||||||||||
| 言語 | ||||||||||||||
| 言語 | eng | |||||||||||||
| 資源タイプ | ||||||||||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||||||||||
| 資源タイプ | journal article | |||||||||||||
| ID登録 | ||||||||||||||
| ID登録 | 10.24517/00027539 | |||||||||||||
| ID登録タイプ | JaLC | |||||||||||||
| 著者 |
Iida, Noriho
× Iida, Noriho× Nakamoto, Yasunari× Baba, Tomohisa× Kakinoki, Kaheita× Li, Ying-Yi× Wu, Yu× Matsushita, Kouji× Kaneko, Shuichi× Mukaida, Naofumi |
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| 著者別表示 |
中本, 安成
× 中本, 安成
× 馬場, 智久
× 金子, 周一
× 向田, 直史
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| 提供者所属 | ||||||||||||||
| 内容記述タイプ | Other | |||||||||||||
| 内容記述 | 金沢大学がん研究所がん病態制御 | |||||||||||||
| 書誌情報 |
Journal of Leukocyte Biology 巻 84, 号 4, p. 1001-1010, 発行日 2008-10-01 |
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| ISSN | ||||||||||||||
| 収録物識別子タイプ | ISSN | |||||||||||||
| 収録物識別子 | 0741-5400 | |||||||||||||
| ISSN | ||||||||||||||
| 収録物識別子タイプ | ISSN | |||||||||||||
| 収録物識別子 | 1938-3673 | |||||||||||||
| NCID | ||||||||||||||
| 収録物識別子タイプ | NCID | |||||||||||||
| 収録物識別子 | AA10641153 | |||||||||||||
| DOI | ||||||||||||||
| 関連タイプ | isVersionOf | |||||||||||||
| 識別子タイプ | DOI | |||||||||||||
| 関連識別子 | 10.1189/jlb.1107791 | |||||||||||||
| 出版者 | ||||||||||||||
| 出版者 | Oxford University Press | |||||||||||||
| 抄録 | ||||||||||||||
| 内容記述タイプ | Abstract | |||||||||||||
| 内容記述 | The first step in the generation of tumor immunity is the migration of dendritic cells (DCs) to the apoptotic tumor, which is presumed to be mediated by various chemokines. To clarify the roles of chemokines, we induced apoptosis using suicide gene therapy and investigated the immune responses following tumor apoptosis. We injected mice with a murine hepatoma cell line, BNL 1ME A.7R.1 (BNL), transfected with HSV-thymidine kinase (tk) gene and then treated the animals with ganciclovir (GCV). GCV treatment induced massive tumor cell apoptosis accompanied with intratumoral DC infiltration. Tumor-infiltrating DCs expressed chemokine receptors CCR1 and CCR5, and T cells and macrophages expressed CCL3, a ligand for CCR1 and CCR5. Moreover, tumor apoptosis increased the numbers of DCs migrating into the draining lymph nodes and eventually generated a specific cytotoxic cell population against BNL cells. Although GCV completely eradicated HSV-tk-transfected BNL cells in CCR1-, CCR5-, or CCL3-deficient mice, intratumoral and intranodal DC infiltration and the subsequent cytotoxicity generation were attenuated in these mice. When parental cells were injected again after complete eradication of primary tumors by GCV treatment, the wild-type mice completely rejected the rechallenged cells, but the deficient mice exhibited impairment in rejection. Thus, we provide definitive evidence indicating that CCR1 and CCR5 and their ligand CCL3 play a crucial role in the regulation of intratumoral DC accumulation and the subsequent establishment of tumor immunity following induction of tumor apoptosis by suicide genes. © Society for Leukocyte Biology.全文公開200910 | |||||||||||||
| 内容記述 | ||||||||||||||
| 内容記述タイプ | Other | |||||||||||||
| 内容記述 | Embargo Period 12 months | |||||||||||||
| 著者版フラグ | ||||||||||||||
| 出版タイプ | AM | |||||||||||||
| 出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||||||||||
| 関連URI | ||||||||||||||
| 識別子タイプ | DOI | |||||||||||||
| 関連識別子 | http://dx.doi.org/10.1189/jlb.1107791 | |||||||||||||
| 関連URI | ||||||||||||||
| 識別子タイプ | URI | |||||||||||||
| 関連識別子 | https://jlb.onlinelibrary.wiley.com/journal/19383673 | |||||||||||||
