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American Journal of Pathology, Vol 137, 393-401, Copyright © 1990 by American Society for Investigative Pathology
REGULAR ARTICLES |
R Takano, M Nose, H Kanno, T Nishihira, S Hiraizumi, A Kobata and M Kyogoku
Department of Pathology, Tohoku University School of Medicine, Sendai, Japan.
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.
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