Thymic Peptides Inhibit Nuclear Factor Kappa B Activation in Human T Lymphocytes

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Abstract
Nuclear factor kappa B (NF-kB), which has been implicated in the regulation of gene transcription, is essential for the expression of genes controlled by the long terminal repeat of human immunodeficiency virus type 1. Studies have shown that reactive oxygen species are involved in signal transduction pathways leading to NF-kB activation. We have reported that calf thymic peptides (TP) protect various cell types from oxidant injury. In this study, we determined the effects of TP on NF-d activation in human T lymphocytes (Jurkat cells) induced by two stimuli: tumor necrosis factor a and phorbol 12-myristate 13-acetate. Activated NF-kB in nuclear extracts was measured by an electrophoretic mobility shift assay (EMSA) using 32P-labeled probe. TP consistently exhibited a dose-dependent inhibition of NF-kB activation induced by both stimuli. Supershift with specific antibodies to NF-kB subunits confirmed that the inducible retarded bards observed in the EMSA are p6.5-p50 heterodimer of the NF-kB/Rel protein. Our data suggest that TP may act via antioxidant mechanisms to block NF-kB activation in Jurkat cells.