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    Lymphokine activated killing of fresh human leukaemias.

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    Authors
    Dawson, M
    Johnston, D
    Taylor, G
    Moore, Michael
    Affiliation
    Department of Immunology, Paterson Laboratories, Christie Hospital and Holt Radium Institute, Manchester M20 9BX.
    Issue Date
    1986
    
    Metadata
    Show full item record
    Abstract
    The relative susceptibility of 10 human leukaemias comprising acute phase leucocytes from 5 acute myeloid and 5 lymphoid neoplasms, and 2 immunoblastic lymphomas to killing by peripheral blood mononuclear cells (PBMC), before and after target cell treatment with phytohaemagglutinin (PHA), and by interleukin-2 (IL-2) activated peripheral blood lymphocytes (PBL) was investigated in short term 51Cr release assays using effector cells from 10 allogeneic donors. Optimal lectin-dependent cellular cytotoxicity (LDCC) was verified against K562 and L1210 cells and lymphokine-activated killing (LAK) against K562 and Daudi cells. Under these conditions, the majority of the leukaemias tested revealed only a finite sensitivity to any of the cytotoxic mechanisms, which was dependent on the donor origin of the effectors. The leukaemias were more consistently susceptible to LDCC than LAK and removal of adherent cells to enrich for the latter activity in effector populations, was ineffective. Lymphocytes from a patient in long term (greater than 5 yr) remission exhibited LAK against the autologous target E84, a natural killer (NK)-sensitive acute myelomonocytic leukaemia. These cells failed to cross-compete for lysis of K562 by LAK cells, suggesting the existence of different recognition structure(s) on the two targets.
    Citation
    Lymphokine activated killing of fresh human leukaemias. 1986, 10 (6):683-8 Leuk Res
    Journal
    Leukemia Research
    URI
    http://hdl.handle.net/10541/116742
    DOI
    10.1016/0145-2126(86)90273-0
    PubMed ID
    3487007
    Type
    Article
    Language
    en
    ISSN
    0145-2126
    ae974a485f413a2113503eed53cd6c53
    10.1016/0145-2126(86)90273-0
    Scopus Count
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    All Paterson Institute for Cancer Research

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