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B/Rel Participation in the Lymphokine-Dependent Proliferation of T Lymphoid Cells1
*
Department of Microbiology and Immunology, Vanderbilt University Medical School, Nashville, TN 37232; and
Immunology Department, Holland Labs, American Red Cross, Bethesda, MD 20855
Proliferative responses of lymphoid cells to IL-2 and IL-4 depend
on activation of the cells, but the mechanism(s) by which activation
enhances cellular competence to respond to cytokines is not fully
understood. The NF-
B/Rel family represents one signal transduction
pathway induced during such activation. We show in this study that
inhibition of NF-B through the expression of an IB
(inhibitory
protein that dissociates from NF-B) mutant refractory to
signal-induced degradation (IB(
N)) interfered with the
acquisition of competence to proliferate in response to IL-4 as well as
IL-2. Thymocytes and T cells from IB(N) transgenic mice
expressed normal levels of IL-2R subunits. However, transgenic cells
exhibited a dramatic defect in Stat5A activation treatment with IL-2,
and a similar defect was observed for IL-4-induced Stat5. In contrast,
T lymphoid cells with inhibition of NF-B showed normal insulin
receptor substrate-2 phosphorylation and only a modest decrease in
Stat6 activation and insulin receptor substrate-1 phosphorylation after
IL-4 stimulation. These results indicate that the NF-B/Rel/IB
system can regulate cytokine receptor capacitation through effects on
the induction of downstream signaling by the Stat transcription factor
family.
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