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    In vitro augmentation of human natural cytotoxic activity.

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    Authors
    Potter, M R
    Moore, Michael
    Affiliation
    Immunology Division, Paterson Laboratories, Christie Hospital and Holt Radium Institute, Manchester, UK
    Issue Date
    1981-05
    
    Metadata
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    Abstract
    Stimulation of human blood lymphocyte preparations with mitomycin C-treated lymphoid cell lines produced increased levels of cytotoxicity against both NK-susceptible and NK-resistant target cell lines. The greatest effect was seen following stimulation by the B lymphocyte-derived lines, Bri8 and raji. K562 also stimulated high levels of activity while the T lymphocyte-derived lines, CCRF/CEM and MOLT 4, produced smaller increases activity was also found in PHA- and MLC-stimulated populations. Stimulation by lymphoid cell lines gave increased cytotoxic activity against all five cell lines when used as target cells and the pattern of target cell susceptibility was maintained, with K562, CCRF/CEM and MOLT 4 being more susceptible than Bri8 and Raji. No direct correlation was found between the level of cytotoxic activity and the level of 3H-thymidine uptake in stimulated effector cell populations. The B cell lines stimulated high levels of isotopic uptake, while the T cell lines gave no significant stimulation. Similarly, the level of 3H-thymidine incorporation following PHA and MLC stimulation showed no direct correlation with the level of cytotoxic activity. Stimulation of lymphocyte transformation did not appear to be necessary for the induction of cytotoxic activity, although the largest increases in cytotoxicity occurred in populations showing high isotope incorporation. No correlation was found between the target cell susceptibility of the different cell lines and their ability to stimulate cytotoxicity.
    Citation
    In vitro augmentation of human natural cytotoxic activity. 1981, 44 (2):332-41 Clin Exp Immunol
    Journal
    Clinical and Experimental Immunology
    URI
    http://hdl.handle.net/10541/135900
    PubMed ID
    7307338
    Type
    Article
    Language
    en
    ISSN
    0009-9104
    Collections
    All Paterson Institute for Cancer Research

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