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B
Degradation1
Departments of
*
Medicine (Rheumatology) and
Microbiology/Immunology, Vanderbilt University Medical School, Nashville, TN 37232; and
Department of Pathology, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA 02115
Although the transcriptional basis for states of unresponsiveness
in primary T cells is unclear, tolerant B lymphocytes exhibit
inhibition of both c-Jun N-terminal kinase induction and I
B
(inhibitor of NF-B) degradation, leading to lower levels of both
nuclear AP-1 and NF-B. Expression of an IB mutant resistant to
signal-induced degradation in transgenic T cells caused markedly
deficient effector cytokine (IL-4, IFN-
) production after primary
TCR stimulation despite a detectable level of nuclear NF-B. A TCR
response element from the IFN- promoter, despite lacking detectable
NF-B/Rel sites, was also unresponsive to TCR ligation. Nuclear
induction of AP-1 proteins in response to T cell activation was
diminished in transgenic T cells. Costimulation induced by
anti-CD28 mAb increased IL-2 production, but failed to reverse the
defects in effector cytokine production. Taken together, these data
indicate that impaired NF-B/Rel signaling in T cells interferes with
the signal transduction pathways required for efficient induction of
effector cytokine production.
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