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B1
Center for Immunology and Cancer Research, University of Queensland, Princess Alexandra Hospital, Brisbane, Queensland, Australia
An understanding of the biochemical control of dendritic cell (DC)
differentiation/activation is essential for improving T cell immunity
by various immunotherapeutic approaches, including DC immunization.
Ligation of CD40 enhances DC function, including conditioning for CTL
priming. NF-
B, and particularly RelB, is an essential control
pathway for myeloid DC differentiation. Furthermore, RelB regulates B
cell Ag-presenting function. We hypothesized that CD40 ligand (CD40L)
and TNF-
, which differ in their capacity to condition DC, would also
differ in their capacity to activate NF-B. DC differentiated for 2
days from monocytes in the presence of GM-CSF and IL-4 were used as a
model, as NF-B activity was constitutively low. The capacity of DC
to activate T cells following CD40L treatment was enhanced compared
with TNF- treatment, and this was NF-B dependent. Whereas
RelB/p50 translocation induced by TNF- was attenuated after 6
h, RelB/p50 nuclear translocation induced by CD40L was sustained for at
least 24 h. The mechanism of this difference related to enhanced
degradation of IB following CD40L stimulation. However, NF-B
activation induced by TNF- could be sustained by blocking autocrine
IL-10. These data indicate that NF-B activation is essential for T
cell activation by DC, and that this function is enhanced if DC NF-B
activation is prolonged. Because IL-10 moderates DC NF-B activation
by TNF-, sustained NF-B activation can be achieved by blocking
IL-10 in the presence of stimuli that induce
TNF-.
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