Expression of costimulatory molecules, B7-1 and B7-2 on human gastric carcinoma

被引:36
|
作者
Koyama, S [1 ]
Maruyama, T
Adachi, S
Nozue, M
机构
[1] Univ Tsukuba, Inst Clin Med, Dept Internal Med, Tsukuba, Ibaraki 3058575, Japan
[2] Univ Tsukuba, Inst Clin Med, Dept Surg, Tsukuba, Ibaraki 3058575, Japan
关键词
costimulating molecule; B7-1(CD80); B7-2(CD86); gastric carcinoma;
D O I
10.1007/s004320050187
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Costimulation of T cells via B7-1 and B7-2 molecules on a tumor has been shown to be important for eliciting cell-mediated antitumor immunity. We studied the surface expression of B7-1 and B7-2 in 24 cases of gastric carcinoma from the primary locus, 20 cases of metastatic carcinoma from malignant ascites, 20 cases of benign gastric mucosa and 7 gastric carcinoma cell lines by two-color flow cytometry with mAb CD80 and CD86. The B7-1 and B7-2 molecules were expressed by 6 cell lines, and I cell line showed the predominant expression of B7-2 but not B7-1. Almost all patients with primary gastric carcinoma and benign gastric mucosa showed high levels of expression of the B7-1 and B7-2, revealing approximately 40%-60% positive cells. However, the percentage of B7-1-positive cells of poorly differentiated primary carcinomas was significantly lower than that of well-differentiated carcinoma and normal mucosa (P<0.01). Furthermore, all of the metastatic carcinoma cells revealed consistently very low or undetectable levels of expression of the B7-1 molecule, only 8 % (mean) of cells being positive, despite showing higher levels of B7-2 expression. Thus, it seems likely that decreased or deleted expression of B7-1 correlates with the grade of tumor differentiation, tumor progression and metastasis. These results suggest that the B7-1 molecule on the gastric carcinoma bearing CD80(+)CD86(+) is abrogated during tumor invasion and/or metastasis, and the turner finally acquires the CD80(-)CD86(+) phenotype. Consequently, inadequate B7-1 costimulation may contribute to the escape of tumors from destruction by the host's immune system.
引用
收藏
页码:383 / 388
页数:6
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