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Immunology |
B Kinase-dependent Mechanism1
Department of Medicine and The Lung Cancer Research Program [R. K. B., Y. L., S. S., M. D., J. L., M. P., S. M. D.], Jonsson Comprehensive Cancer Center [R. K. B., S. M. D.], University of California at Los Angeles and Veterans Administration-Greater Los Angeles Health Care System, Los Angeles, California 90095
T lymphocyte survival is critical for the development and maintenance of an effective host antitumor immune response; however, the tumor environment can negatively impact T-cell survival. Lymphocytes exposed to tumor supernatants (TSNs) were evaluated for apoptosis after mitogen stimulation. TSN was observed to significantly enhance phorbol 12-myristate 13-acetate/ionomycin- and anti-CD3-stimulated lymphocyte apoptosis. Enhanced lymphocyte apoptosis was associated with an impairment of nuclear factor
B nuclear translocation and diminished I
B
degradation. In lymphocytes stimulated after exposure to TSNs, cytoplasmic I
B
persisted as a result of alterations in I
B kinase (IKK) activity. Accordingly, although there were no apparent differences in IKK component concentrations, lymphocytes preexposed to TSNs exhibited markedly reduced IKK activity. We conclude that non-small cell lung cancer-derived soluble factors promote apoptosis in activated lymphocytes by an IKK-dependent pathway.
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