Takano R, Nose M, Kanno H, Nishihira T, Hiraizumi S, Kobata A, Kyogoku M
Department of Pathology, Tohoku University School of Medicine, Sendai, Japan.
Am J Pathol. 1990 Aug;137(2):393-401.
Cell-to-cell contact between macrophages and tumor cells is an important initial reaction in a host defense mechanism against tumor cells. The authors have studied cell surface components of human esophageal carcinoma cells recognized by macrophages. Superoxide release from THP-1 cells, a human macrophage cell line, was analyzed in their interaction with a battery of human squamous cell carcinoma cell lines (TE) originated from esophageal cancer patients. The macrophage-triggering ability of TE 1 cell line, a high stimulant, was reduced after treatment with trypsin or tunicamycin, an inhibitor of N-glycosidic glycosylation. Addition of monosaccharides was efficient in competitive inhibition of these cellular interaction. Moreover, con-A-resistant mutation of TE 1 cells was found to reduce their macrophage-triggering ability, associated with increase of L-PHA-binding capacity, suggesting substitution to the GlcNAc beta(1----6)-linked lactosamine antenna in N-glycosidic carbohydrates. These findings suggest that terminal residues of N-glycosidic carbohydrates on some esophageal carcinoma cells may contribute to the recognition sites of macrophages.
巨噬细胞与肿瘤细胞之间的细胞间接触是宿主抗肿瘤细胞防御机制中的重要初始反应。作者研究了巨噬细胞识别的人食管癌细胞的细胞表面成分。分析了人巨噬细胞系THP-1细胞与一系列源自食管癌患者的人鳞状细胞癌细胞系（TE）相互作用时的超氧化物释放情况。高刺激物TE 1细胞系的巨噬细胞触发能力在用胰蛋白酶或N-糖苷糖基化抑制剂衣霉素处理后降低。添加单糖可有效竞争性抑制这些细胞间相互作用。此外，发现TE 1细胞的刀豆球蛋白A抗性突变会降低其巨噬细胞触发能力，并伴有L-植物血凝素结合能力的增加，提示N-糖苷碳水化合物中GlcNAc β(1----6)-连接的乳糖胺天线发生了取代。这些发现表明，某些食管癌细胞上N-糖苷碳水化合物的末端残基可能有助于巨噬细胞的识别位点。
