Accelerated tumor growth in mice deficient in DNAM-1 receptor.
Accelerated tumor growth in mice deficient in DNAM-1 receptor.
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DOI：
10.1084/jem.20081611
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发表时间：
2008-12-22
期刊：
影响因子：
--
通讯作者：
Shibuya A
中科院分区：
文献类型：
--
作者：
Iguchi-Manaka A;Kai H;Yamashita Y;Shibata K;Tahara-Hanaoka S;Honda S;Yasui T;Kikutani H;Shibuya K;Shibuya A
自从人类和小鼠DNAM-1的配体的鉴定以来，新出现的证据表明DNAM-1在T细胞和自然杀伤（NK）细胞介导的肿瘤细胞的识别和裂解中起重要作用。然而，DNAM-1是否参与体内肿瘤免疫监视仍不确定。我们通过使用DNAM-1缺陷小鼠解决了这个问题。DNAM-1缺陷型细胞毒性T淋巴细胞（CTL）和NK细胞在体外对表达DNAM-1配体的肿瘤的细胞毒性活性明显低于野生型（WT）细胞。甲基胆蒽（MCA）诱导的纤维肉瘤细胞系Meth A表达DNAM-1配体CD 155，DNAM-1缺陷小鼠移植Meth A细胞后肿瘤发展和死亡率增加。此外，与WT小鼠相比，DNAM-1缺陷小鼠分别对化学致癌物MCA和7，12-二甲基苯并[a]蒽（DMBA）产生了显着更多的DNAM-1配体表达纤维肉瘤和乳头状瘤细胞。这些结果表明DNAM-1在肿瘤发展的免疫监视中起重要作用。
Since the identification of ligands for human and mouse DNAM-1, emerging evidence has suggested that DNAM-1 plays an important role in the T cell– and natural killer (NK) cell–mediated recognition and lysis of tumor cells. However, it remains undetermined whether DNAM-1 is involved in tumor immune surveillance in vivo. We addressed this question by using DNAM-1–deficient mice. DNAM-1–deficient cytotoxic T lymphocyte (CTL) and NK cells showed significantly less cytotoxic activity against DNAM-1 ligand-expressing tumors in vitro than wild-type (WT) cells. The methylcholanthrene (MCA)-induced fibrosarcoma cell line Meth A expressed the DNAM-1 ligand CD155, and DNAM-1–deficient mice showed increased tumor development and mortality after transplantation of Meth A cells. Moreover, the DNAM-1–deficient mice developed significantly more DNAM-1 ligand-expressing fibrosarcoma and papilloma cells in response to the chemical carcinogens MCA and 7,12-dimethylbenz[a]anthracene (DMBA), respectively, than did WT mice. These results indicate that DNAM-1 plays an important role in immune surveillance of tumor development.
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影响因子：
11.2
作者：
Carlsten, Mattias;Bjorkstrom, Niklas K.;Malmberg, Karl Johan
通讯作者：
Malmberg, Karl Johan
DOI：
10.2174/1568014053005390
发表时间：
2005-02-01
期刊：
Current Medicinal Chemistry - Anti-Inflammatory & Anti-Allergy Agents
影响因子：
--
作者：
Shibuya, Akira;Tahara-Hanaoka, Satoko;Shibuya, Kazuko
通讯作者：
Shibuya, Kazuko
影响因子：
4.8
作者：
Kojima, H;Kanada, H;Shibuya, A
通讯作者：
Shibuya, A
影响因子：
4.4
作者：
Cretney, E;Takeda, K;Smyth, MJ
通讯作者：
Smyth, MJ
影响因子：
24.5
作者：
Masson, D;Jarry, A;Denis, MG
通讯作者：
Denis, MG