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B-Dependent Transcription in T Lymphocytes1
Department of Microbiology and Immunology, University of Tampere Medical School, Tampere, Finland
Reactive oxygen species (ROS) are used as signaling molecules in T
cell activation. One of the main targets of ROS is the transcription
factor nuclear factor-
B (NF-B). NF-B-dependent transcription
is inhibited by antioxidants, and the activation is induced or
potentiated by ROS. However, chronic oxidative stress is known to
reduce the activation of T cells and NF-B. To analyze these
phenomena in more detail, we have exposed Jurkat T cells in vitro to
oxidative stress (H2O2) at various times
before or simultaneously with signals known to activate NF-B
(phorbol dibutyrate (PDBu) and TNF). Simultaneously applied
H2O2 strongly potentiated the PDBu- or
TNF-induced transcriptional activity of NF-B. In contrast to this,
H2O2 given 3 to 20 h before the activating
signal reduced NF-B-dependent transcriptional activity. This was not
due to the oxidation-induced modification of NF-B; cytoplasmic
NF-B was able to bind to DNA after dissociation from IB
by
detergent treatment. H2O2 pre-exposure
effectively inhibited the PDBu- or TNF-induced phosphorylation and
degradation of IB, but H2O2 given
simultaneously with PDBu or TNF enhanced the degradation. Oxidative
stress was also followed by a strongly decreased ability to form
intracellular ROS. Taken together, these data indicate that IB
phosphorylation is the target of action of ROS, and as the ROS-forming
capacity is weaker after chronic oxidative stress, IB is not
effectively phosphorylated and degraded, thus leading to decreased
NF-B-dependent transcription.
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