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Transplantationslabor, Klinik für Abdominal- und Transplantationschirurgie, Medizinische Hochschule Hannover,
Abteilung für Molekulare Pathologie, Universität Würzburg, Würzburg; and
Hoechst-Marion-Roussel, Wiesbaden, Germany
Stimulation of resting human T cells with the CD28-specific mAb BW
828 induces proliferation and cytokine synthesis without further
requirement for TCR coengagement. This observation prompted us to
postulate that signal 2 (costimulatory signal) alone without signal 1
(TCR signal) can activate T cells. To test whether this putative
function of CD28 is mediated via a particular signaling pathway, we
compared early signaling events initiated in resting T cells by the
stimulatory mAb BW 828 with signals triggered by the nonstimulating
CD28 mAb 9.3. Stimulation of T cells with BW 828 induced an increase in
intracellular Ca2+, but did not lead to detectable
activation of the protein kinases p56lck
and c-Raf-1. This pathway resulted in the induction of the
transcription factors NF-
B, NF-AT, and proteins binding to the CD28
response element of the IL-2 promoter. On the other hand, stimulation
of T cells with mAb 9.3 increased the level of intracellular
Ca2+ and triggered the activation of
p56lck and c-Raf-1, but was unable to
induce the binding of transcription factors to the IL-2 promoter. In
contrast to the differential signaling of BW 828 and 9.3 in resting T
cells, the two mAbs exhibited a similar pattern of early signaling
events in activated T cells and Jurkat cells
(p56lck activation, association of
phosphatidylinositol 3-kinase with CD28), indicating that the signaling
capacity of CD28 changes with activation. These data support the view
that stimulation through CD28 can induce some effector functions in T
cells and suggest that this capacity is associated with a particular
pattern of early signaling events.
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