| Summary: | 碩士 === 國立臺灣大學 === 免疫學研究所 === 84 === The activation of T cellsrequirs two signals. The first is
delivered form the TCR/CD3 complx and the second signal is tri-
ggered by accessory molecules on APC.The CD28 signaling is the
most potent costimulatory pathway identified to date. However,
ligation of the TCR complex on previously activated T cells and
T cell line has been shown to result in activation-induced cell
death (AICD) through apoptosis. This mechanism of homeostasis
maintains the numbers and function of T cells.
AICD is belived to play a centrol role in the homeostatic
regulation of immune response. It is suggested that Fas and Fas
ligand interaction play an important role in inducing AICD.How-
ever,AICD can also be induced in peripheral T cell of lpr/lpr
mice. In addition to Fas and FasL,other molecules may also exist
to participate the deletion of activated T in peripheral system.
Furthermore,not all previously activated T cells undergo apopto-
sis after activation.So,the mechanism controlling the differen-
tial susceptibility of T cells to AICD is still not clear.
Cross-linking of CD28 has no effect on bcl-2 gene expression,but
can augment the expression of bcl-xL gene.Therefore we have
investigated whether CD28 costimulation can prevent T cell AICD.
We identify,herein,a novel function of murine CD28 in the
regulation of activation-induced cell death by in vitro cell
culture system.Our data shown that addition of anti-CD28mAb can
prevent the primary activated splenic T cells from apoptosis
induced by recross-linking of TCR/CD3 complex.Furtherly,we find
that the TNF-R2 cross-Linking can induces a death signal to T
cells at 48 hours after activation.However,antibodies to CD28,
when cross-linked,greatly inhibited apoptosis via TNF-R2.
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