Department of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Cancer Sci. 2013 Jul;104(7):945-51. doi: 10.1111/cas.12167. Epub 2013 May 9.
In several malignant tumors including lymphoma, macrophages that infiltrate tumor tissues are called tumor-associated macrophages (TAMs). We discovered that TAMs, especially the CD163⁺ alternatively activated phenotype (M2), were closely involved with progression of adult T-cell leukemia/lymphoma (ATLL). We used CD68 (a pan-macrophage marker) and CD163 (an M2 marker) to immunostain 58 ATLL samples. Statistical analyses showed that a high number of CD68⁺ TAMs and an increased percentage of CD163⁺ cells among the TAMs were associated with a worse clinical prognosis; multivariate analysis indicated that the percentage of CD163⁺ cells was an independent prognostic factor. We also carried out in vitro coculture experiments with ATLL cell lines (ATN-1 and TL-Mor) and monocyte-derived macrophages and found that direct coculture with M2 macrophages significantly increased BrdU incorporation into ATLL cell lines. A cytokine array analysis showed that macrophage-derived soluble factors including C5a, tumor necrosis factor-α, growth-related oncogene-α, CCL1/I-309, and interleukin-6 stimulated ATLL cell lines. CD163 expression in macrophages was strongly induced by direct contact with ATN-1 cells, and downregulation of CD163 in macrophages significantly suppressed growth of cocultured ATN-1 cells. These results suggest that interaction between M2 macrophages and lymphoma cells may be an appropriate target in treatment of patients with ATLL.
在包括淋巴瘤在内的几种恶性肿瘤中,浸润肿瘤组织的巨噬细胞被称为肿瘤相关巨噬细胞(TAMs)。我们发现 TAMs,尤其是 CD163⁺ 替代激活表型(M2),与成人 T 细胞白血病/淋巴瘤(ATLL)的进展密切相关。我们使用 CD68(一种泛巨噬细胞标志物)和 CD163(一种 M2 标志物)对 58 个 ATLL 样本进行免疫染色。统计分析表明,高数量的 CD68⁺ TAMs 和 TAMs 中 CD163⁺ 细胞的百分比增加与更差的临床预后相关;多变量分析表明,CD163⁺ 细胞的百分比是一个独立的预后因素。我们还进行了 ATLL 细胞系(ATN-1 和 TL-Mor)与单核细胞衍生的巨噬细胞的体外共培养实验,发现与 M2 巨噬细胞的直接共培养显著增加了 BrdU 掺入 ATLL 细胞系。细胞因子阵列分析表明,巨噬细胞衍生的可溶性因子,包括 C5a、肿瘤坏死因子-α、生长相关癌基因-α、CCL1/I-309 和白细胞介素-6,刺激了 ATLL 细胞系。巨噬细胞中的 CD163 表达在与 ATN-1 细胞直接接触时被强烈诱导,巨噬细胞中 CD163 的下调显著抑制了共培养的 ATN-1 细胞的生长。这些结果表明,M2 巨噬细胞与淋巴瘤细胞之间的相互作用可能是治疗 ATLL 患者的一个合适靶点。