Cell surface N-linked sugars may play a role in target cell recognition by cytotoxic T lymphocytes (CTL). We have studied this role by treating tumor cell targets with tunicamycin, an effective inhibitor of N-linked glycosylation in mammalian cells. We determined a tunicamycin treatment protocol in which glycosylation was blocked and in which target cell killing by 5-day primary mixed lymphocyte reaction CTL was inhibited, yet in which cell viability was high and expression of major histocompatibility complex molecules was normal. It was found that tunicamycin-treated cells were killed only about one-half as well as untreated targets and that tunicamycin-treated target cells were less effective than untreated target cells as cold target competitors in cold target competition experiments. These observations suggest that for optimal killing, CTL require an interaction with the target cell that involves N-linked glycans on the target cell surface.

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