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Lymphokine-Activated Killer Cells Can Kill Target Cells Not Only by Early Killing But Also by Late Killing, and the Late Killing Level Against Autotumor Cell Line

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Generally, lymphokine-activated killer (LAK) cells kill target cells early after the LAK cells adhere to them. In this study, we describe that LAK cells can also kill at a later time, such as 24–96 h. LAK cells were generated from a cancer patient and healthy volunteers. As target cells, the patient's autotumor cell line H41 was used. When LAK cells were added to the target cells in a culture well, the LAK cells killed the target cells by cell–cell adhesion within 1–4 h (early killing), but not all cells were killed. The LAK cells were then removed. However, the remaining cells ultimately died 24–96 h later (late killing). The late killing was different from the early killing because numerous granules and vacuoles appeared in the cytoplasm. The late killing was not induced by adding supernatant of the LAK cell culture, suggesting that LAK–target cell contact may be necessary for the killing. The cell injury was inhibited by 3-methyladenine (lysosome inhibitor). It suggests that the vacuoles may be caused by activated lysosome. The patient’s LAK cells induced late killing at high levels. There was a high percentage of CD8+CD16+ cells in the peripheral blood lymphocytes (PBL). This subset induced late killing more effectively than the CD8-CD16+ subset. Killing was more conspicuous against H41 than against allogeneic cell line T98G. This type of killing is noteworthy for understanding of killing mechanism of LAK cells.
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Keywords: Key words: LAK cells; Early killing; Cell–cell adhesion killing; Late killing; Autotumor cell line; Lysosome

Document Type: Research Article

Affiliations: Department of Clinical Physiology, Kagawa Nutrition University, 3-9-21 Chiyoda, Sakado, Saitama 350-0288, Japan2

Publication date: 2002-01-01

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