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The Journal of Immunology, Vol 132, Issue 4 2021-2029, Copyright © 1984 by American Association of Immunologists
ARTICLES |
P Koppel, E Peterhans, G Bertoni, R Keist, P Groscurth, R Wyler and R Keller
A variety of host cells, such as activated macrophages, natural killer (NK) cells, and polymorphonuclear leukocytes (PMNL), are cytotoxic for an array of non-antibody-coated tumor cells. Because such effector cells appear to use oxygen-dependent mechanisms to effect tumor cell destruction in certain systems, the possibility of an involvement of toxic oxygen species has been considered. To investigate whether interaction of effector cells with neoplastic cells induces the generation of reactive oxygen species, resting and activated rat macrophages and rat spleen cells (as a source of NK activity) were exposed to viable tumor cells of varied origin, and chemiluminescence was monitored. This sensitive indicator of reactive oxygen generation was stimulated only when tumor cells or culture supernatants were contaminated with mycoplasma. Mycoplasma-free tumor cells and culture supernatants were in no case able to trigger chemiluminescence in any of these effector cell populations. On the other hand, tumor targets were equally susceptible to killing by effector cells irrespective of whether mycoplasma were present. The data suggest that generation of chemiluminescence during interaction of natural cytotoxic cells and neoplastic cells is an artifact and that reactive oxygen species do not function as an effector mechanism in antibody-independent natural killing effected by activated macrophages and NK cells.
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