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Influence of lectin-free interleukin-2 on natural and antibody-dependent cellular cytotoxicity
Supernatants derived from MLA-144, a gibbon T cell line that constitutively releases interleukin-2 (IL-2) and which lack detectable interferon (IFN) had the capacity to enhance the natural killer (NK) cells function of human peripheral blood lymphocytes. Percoll fractionation revealed that like IFN-inducible cytotoxic cells lymphocytes responding to MLA-144 supernatants cofractionate with native NK cells. Exposure to MLA-144 conditioned medium also potentiated the cytotoxic capacity of extravascular effector cells which are either unresponsive or weakly responsive to interferon-alpha (IFN-alpha). Moreover lymphocyte (K cell)-mediated antibody-dependent cellular cytotoxicity (ADCC) which is unresponsive to IFN-alpha was in most cases subject to a modest potentiation following treatment with MLA-144 supernatants. These data confirm previous reports that IL-2 can regulate peripheral blood NK cell function and also demonstrate that this lymphokine can also influence those natural cytotoxic mechanisms which are unresponsive to IFN-alpha.
Supernatants derived from MLA-144, a gibbon T cell line that constitutively releases interleukin-2 (IL-2) and which lack detectable interferon (IFN) had the capacity to enhance the natural killer (NK) cells function of human peripheral blood lymphocytes. Percoll fractionation revealed that like IFN-inducible cytotoxic cells lymphocytes responding to MLA-144 supernatants cofractionate with native NK cells. Exposure to MLA-144 conditioned medium also potentiated the cytotoxic capacity of extravascular effector cells which are either unresponsive or weakly responsive to interferon-alpha (IFN-alpha). Moreover lymphocyte (K cell)-mediated antibody-dependent cellular cytotoxicity (ADCC) which is unresponsive to IFN-alpha was in most cases subject to a modest potentiation following treatment with MLA-144 supernatants. These data confirm previous reports that IL-2 can regulate peripheral blood NK cell function and also demonstrate that this lymphokine can also influence those natural cytotoxic mechanisms which are unresponsive to IFN-alpha.