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Immunology Division, Cancer Research Laboratory, Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720
Although the recently identified ICOS/B7h costimulatory
counterreceptors are critical regulators of CD4+ T cell
responses, their ability to regulate CD8+ responses is
unclear. Here we report using a tumor-rejection model that ectopic B7h
expression can costimulate rejection by CD8+ T cells in the
absence of CD4+ T cells. Although responses of naive T
cells were significantly augmented by priming with B7h, B7h was
surprisingly effective in mobilizing recall responses of adoptively
transferred T cells. To explore why secondary responses of
CD8+ T cells were particularly enhanced by B7h, kinetics of
ICOS up-regulation, proliferative responses, and cytokine production
were compared from both naive and rechallenged 2C-transgenic T cells
costimulated in vitro. Although B7h costimulated proliferative
responses from both CD8+ populations, rechallenged cells
were preferentially costimulated for IL-2 and IFN-
production. These
results indicate that ICOS/B7h counterreceptors likely function in vivo
to enhance secondary responses by CD8+ T
cells.
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