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Department of Pathology and Microbiology, University of Bristol School of Medical Sciences, Bristol, United Kingdom
The CD28/B7 system provides costimulatory signals necessary for
optimal T cell activation. We have examined the effects of blocking
B7.1 and/or B7.2 in an in vitro system using TCR transgenic T cells
specific for myelin basic protein. Activation of naive T cells was
found to be B7.2 dependent and not dependent on the presence of B7.1
molecules. However, increasing the strength of signal through the TCR
using peptide analogues with higher affinity for MHC compensated for
blockade of B7.2 molecules, suggesting that signal 1 alone can be
sufficient for the activation of naive T cells. The role of B7
molecules in the differentiation of T cells was further investigated by
restimulating T cells with fresh APC and peptide in B7-sufficient
conditions. A down-regulation of IL-2 and IFN-
production by T cells
primed in the presence of anti-B7.2 mAb was partially overcome when
high affinity peptide analogues were used to restimulate T cells. In
contrast, a significant down-regulation of the differentiation of cells
producing Th-2 cytokines was observed in the presence of anti-B7
Abs. Differentiation of IL-4-secreting cells was influenced by both
B7.1 and B7.2, while IL-5 secretion was totally dependent on B7.2.
These results suggest that B7-mediated costimulation is essential for
the development of Th-2-associated cytokines, the absence of which
cannot be overcome by increasing the strength of the signal through the
TCR.
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