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Vol. 62, Issue 3, 722-728, September 2002
and Anti-CD40-Induced Activation of
NF-
B/Rel in Dendritic Cells: p50 Homodimer Activation Is Not
Affected
Department of Environmental and Molecular Toxicology, and
Environmental Health Science Center, Oregon State University,
Corvallis, Oregon
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD)
suppresses many immune responses, both innate and adaptive. Suppression
is mediated by the aryl hydrocarbon receptor (AhR), a ligand-activated
transcription factor. The AhR mediates TCDD toxicity presumably through
the alteration of transcriptional events, either by promoting gene expression or potentially by physically interacting with other transcription factors. Another transcription factor, NF-
B/Rel, is
involved in several signaling pathways in immune cells and is crucial
for generating effective immune responses. Dendritic cells (DCs),
considered to be the "pacemakers" of the immune system, were
recently recognized as targets of TCDD and are also dependent on
NF-B/Rel for activation and survival. In these studies, we investigated whether TCDD would alter the activation of NF-B/Rel in
DCs. The dendritic cell line DC2.4 was exposed to TCDD before treatment
with tumor necrosis factor 
(TNF-) or anti-CD40, and NF-B/Rel
activation was measured by electrophoretic mobility shift assay and
immunoblotting. TCDD suppressed the binding of NF-B/Rel to its
cognate response element in TNF-- and anti-CD40-treated cells and
blocked translocation to the nucleus. The AhR was shown to associate
with RelA, after coimmunoprecipitation, and seemed to block its binding
to DNA. It is noteworthy that p50 homodimers freely bound to DNA. These
results suggest that TCDD may alter the balance between NF-B/Rel
heterodimers and transcriptional inhibitory p50 homodimers in DCs,
leading to defects in the DCs and suppression of the immune response.
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