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J. Biol. Chem., Vol. 269, Issue 48, 30077-30080, 12, 1994
JH Lai and TH Tan
CD28, an important T cell surface molecule, mediates a costimulatory signal
in the activation of T cell immune responses. CD28 signaling is resistant
to the immunosuppressant cyclosporin A (CsA) but sensitive to the
immunosuppressant rapamycin. CD28 costimulation induces transcription from
the interleukin (IL)-2 promoter via the CD28 response element. The levels
of c-Rel, a CD28 response element-binding factor, were found previously to
be increased by CD28 costimulation. Therefore, we focused our present study
on the mechanism(s) of c-Rel up- regulation by CD28 signaling in Jurkat T
cells. In this paper, we showed that CD28 costimulation accelerated the
kinetics of nuclear translocation of c-Rel. We showed that CD28 signaling,
distinct from other stimuli such as phorbol 12-myristate 13-acetate, IL-1,
and tumor necrosis factor-alpha, caused a sustained down-regulation of the
inhibitor I kappa B alpha in Jurkat T cells. However, the levels of two
other c-Rel inhibitors, namely NFKB1 (p105) and NFKB2 (p100), were not
affected. Remarkably, the CD28-mediated down-regulation of I kappa B alpha
was prevented by rapamycin but not by CsA. The counter-regulation of I
kappa B alpha by CD28 signaling and rapamycin observed in Jurkat T cells is
also reproducible in primary T cells. In contrast, the phorbol 12-myristate
13-acetate/ionomycin-mediated down-regulation of I kappa B alpha was
prevented by CsA but not by rapamycin. Our data suggest that I kappa B
alpha is the down-stream target of both CD28 signaling and rapamycin; a
continued down-regulation of I kappa B alpha by CD28 costimulation leads to
enhanced nuclear translocation of c-Rel, which in turn causes a sustained
up-regulation of IL-2 gene expression.
CD28 signaling causes a sustained down-regulation of I kappa B alpha which can be prevented by the immunosuppressant rapamycin
Department of Microbiology and Immunology, Baylor College of Medicine, Houston, Texas 77030.
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