ArticleJournal of clinical immunology1987
T-cell surface molecules involved in the induction and expression of lymphokine-activated killing of autologous and allogeneic tumor targets.
Article in Journal of clinical immunology, 1987. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
The cellular interactions and the surface molecules involved in the generation and the expression of lymphokine-activated killer-cell (LAK) activities in vitro in blood mononuclear cells (BMN) from cancer patients and healthy individuals against autologous and allogeneic tumors were studied. The depletion of a plastic-adherent population(s) from BMN at the initiation of in vitro cultures in recombinant interleukin-2 (rIL-2) markedly interfered with the generation of LAK activities. Readdition of the same number of irradiated autologous plastic-adherent cells to the nonadherent population restored the generation of LAK. The requirement of the plastic-adherent population(s) in in vitro induction of LAK activities was observed only in autologous situations. Furthermore, selective modulations of CD3 and CD2 receptors on BMN with the appropriate monoclonal antibodies (MAb) during the induction phases of LAK responses profoundly inhibited the generation of LAK. Thus, unhindered expression of CD2 molecules and CD3 molecules were necessary for the maximum cytotoxic activation of non-antigen-driven effector cells in short-term cultures in rIL-2.
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