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*
Department of Pathology, Committee on Immunology, and
Department of Medicine, University of Chicago, Chicago, IL 60637;
Department of Immunology, University of Washington, Seattle, WA 98195; and
§
Genetics Institute, Cambridge, MA 02140
Using a TCR transgenic mouse bred onto a recombinase-activating
gene-2-deficient background, we have examined the influence of B7.1 and
B7.2 on activation of naive, CD8+ T cells in vitro. We
found that B7.1 was a more potent costimulus than B7.2 for induction of
proliferation and IL-2 production by naive CD8+ T cells.
This difference appeared to be quantitative in nature, as determined
using transfectants expressing various defined levels of B7.1 or B7.2,
or using purified B7.1 or B7.2 fusion proteins. In contrast to the
quantitative differences seen in stimulation of naive T cells, B7.1 and
B7.2 were comparable in their ability to costimulate responses in T
cells previously primed in vitro. In addition, primed, but not naive, T
cells were capable of proliferating and producing IL-2 in response to a
TCR stimulus alone, apparently in the absence of B7 costimulation.
Lastly, we found that B7.1 and B7.2 were equivalently capable of
driving differentiation of naive CD8+ T cells into an
IL-4-producing phenotype when exogenous IL-4 was added to the primary
culture or to an IFN-
-producing phenotype in the presence of IL-12.
These results indicate that signals generated by B7.1 and B7.2 are
qualitatively similar, but that B7.1 is quantitatively stronger than
B7.2. Further, our results indicate that the activation state of the
responding T cell may influence the efficiency with which the T cell
can respond to a costimulatory signal provided by either B7.1 or
B7.2.
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