Increased CD112 expression in methylcholanthrene-induced tumors in CD155-deficient mice.
Increased CD112 expression in methylcholanthrene-induced tumors in CD155-deficient mice.
复制标题
DOI：
10.1371/journal.pone.0112415
复制
发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Shibuya K
中科院分区：
文献类型：
--
作者：
Nagumo Y;Iguchi-Manaka A;Yamashita-Kanemaru Y;Abe F;Bernhardt G;Shibuya A;Shibuya K
免疫效应细胞的肿瘤识别是由抗原受体和多种粘附和共刺激分子介导的。自从在人类和小鼠中鉴定出CD 155和CD 112作为DNAM-1的配体以来积累的证据表明，DNAM-1及其配体之间的相互作用在T细胞和自然杀伤（NK）细胞介导的肿瘤细胞识别和裂解中起重要作用。我们以前已经证明，甲基胆蒽（MCA）加速肿瘤的发展在DNAM-1缺陷的小鼠，和MCA诱导的肿瘤上的Cd 155水平是显着高于DNAM-1缺陷的小鼠比野生型（WT）小鼠。相比之下，WT和DNAM-1缺陷小鼠肿瘤上的CD 112表达相似，表明CD 155作为DNAM-1配体在活化T细胞和NK细胞进行肿瘤免疫监视中起主要作用。为了解决这一假设，我们研究了MCA诱导的CD 155缺陷小鼠肿瘤的发展。出乎意料的是，我们观察到WT和CD 155缺陷小鼠之间的肿瘤发展没有显著差异。相反，我们发现在MCA诱导的CD 155缺陷小鼠肿瘤中，CD 112的表达显著高于WT小鼠。我们还观察到CD 155缺陷小鼠中CD 8 + T细胞上DNAM-1的表达较高，抑制性受体TIGIT的表达较低。这些结果表明，受体和CD 112的表达的调节补偿了针对MCA诱导的肿瘤的免疫监视中的CD 155缺陷。
Tumor recognition by immune effector cells is mediated by antigen receptors and a variety of adhesion and costimulatory molecules. The evidence accumulated since the identification of CD155 and CD112 as ligands for DNAM-1 in humans and mice has suggested that the interactions between DNAM-1 and its ligands play an important role in T cell– and natural killer (NK) cell–mediated recognition and lysis of tumor cells. We have previously demonstrated that methylcholanthrane (MCA) accelerates tumor development in DNAM-1–deficient mice, and the Cd155 level on MCA-induced tumors is significantly higher in DNAM-1–deficient mice than in wild-type (WT) mice. By contrast, Cd112 expression on the tumors is similar in WT and DNAM-1-deficient mice, suggesting that CD155 plays a major role as a DNAM-1 ligand in activation of T cells and NK cells for tumor immune surveillance. To address this hypothesis, we examined MCA-induced tumor development in CD155-deficient mice. Unexpectedly, we observed no significant difference in tumor development between WT and CD155-deficient mice. Instead, we found that Cd112 expression was significantly higher in the MCA-induced tumors of CD155-deficient mice than in those of WT mice. We also observed higher expression of DNAM-1 and lower expression of an inhibitory receptor, TIGIT, on CD8+ T cells in CD155-deficient mice. These results suggest that modulation of the expression of receptors and CD112 compensates for CD155 deficiency in immune surveillance against MCA-induced tumors.
登录
查看更多内容
DOI：
10.1084/jem.20081611
发表时间：
2008-12-22
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Iguchi-Manaka A;Kai H;Yamashita Y;Shibata K;Tahara-Hanaoka S;Honda S;Yasui T;Kikutani H;Shibuya K;Shibuya A
通讯作者：
Shibuya A
影响因子：
11.2
作者：
Carlsten, Mattias;Bjorkstrom, Niklas K.;Malmberg, Karl Johan
通讯作者：
Malmberg, Karl Johan
影响因子：
5.4
作者：
Maier, Michael K.;Seth, Sebastian;Bernhardt, Guenter
通讯作者：
Bernhardt, Guenter
影响因子：
24.5
作者：
Masson, D;Jarry, A;Denis, MG
通讯作者：
Denis, MG
影响因子：
4.8
作者：
Seth, Sebastian;Qiu, Quan;Bernhardt, Guenter
通讯作者：
Bernhardt, Guenter