Difference in immunosuppressive cells between the peritumoral area and tumor core in glioblastoma.

Difference in immunosuppressive cells between the peritumoral area and tumor core in glioblastoma.
复制标题

胶质母细胞瘤瘤周区域和肿瘤核心之间免疫抑制细胞的差异。

DOI:
10.1016/j.wneu.2018.08.133
复制
发表时间:
2018
期刊:
影响因子:
2
通讯作者:
Toda M
Toda M
中科院分区:
医学4区
文献类型:
--
作者:
Tamura R;Ohara K;Sasaki H;Morimoto Y;Kosugi K;Yoshida K;Toda M

文献摘要

相似文献

血管内皮生长因子(VEGF)-A和VEGF受体在胶质母细胞瘤瘤周脑区(PBZ)的表达与肿瘤核心(TC)的表达不同。到目前为止,还没有比较研究研究免疫抑制细胞在胶质母细胞瘤PBZ和TC中的表达。方法采用免疫组化方法分析10例新诊断的胶质母细胞瘤患者外周血中VEGF-A、缺氧诱导因子-1α、程序性细胞死亡-1 (PD-1)、Foxp3、CD163、CD4和CD8的表达,评价其免疫抑制微环境。结果TC组Foxp3+和CD163+细胞数量明显高于PBZ组,并与TC组缺氧诱导因子-1α和VEGF-A表达显著高于PBZ组相关。TC中CD8+T细胞数量低于PBZ, TC中PD-1+CD8+T细胞数量高于PBZ。这些结果表明,缺氧条件可能与淋巴细胞上PD-1的表达、Foxp3+调节性T细胞和CD163+肿瘤相关巨噬细胞的分布有关。结论本研究首次报道了胶质母细胞瘤TC区和PBZ区免疫抑制细胞和免疫检查点分子表达差异的临床病理特征。
BackgroundVascular endothelial growth factor (VEGF)-A and VEGF receptor expression in the peritumoral brain zone (PBZ) differs from that in the tumor core (TC) of glioblastoma. To date, no comparative study has investigated the expression of immunosuppressive cells in the PBZ and TC of glioblastoma.MethodsIn 10 patients with newly diagnosed glioblastoma, we used immunohistochemistry to analyze the expression of VEGF-A, hypoxia-inducible factor-1α, programmed cell death-1 (PD-1), Foxp3, CD163, CD4, and CD8 to assess the immunosuppressive microenvironment.ResultsThe number of Foxp3+and CD163+cells was significantly greater in the TC than in the PBZ and correlated with greater expression of hypoxia-inducible factor-1α and VEGF-A in the TC than in the PBZ. The number of CD8+T cells was lower in the TC than in the PBZ, and the TC had more PD-1+CD8+T cells compared with the PBZ. These results suggest that the hypoxic condition could be associated with PD-1 expression on lymphocytes, the distribution of Foxp3+regulatory T cells and CD163+tumor-associated macrophages.ConclusionsThe present study reports the first clinicopathologic features of the differences in immunosuppressive cells and the expression of immune checkpoint molecules between the TC and PBZ of glioblastoma.