The purpose of this study was to examine the role of
IL-1 on the activation of CD8+/CD4- class I-restricted helper cell-independent cytolytic T cell (
HITc) clones known to produce
IL-2 and proliferate in vitro after Ag stimulation with a Friend retrovirus-induced
leukemia (FBL). The functional role of
IL-1 in Ag-specific proliferation and
IL-2 secretion was assessed by stimulating the T cell clones with FBL either in the presence or absence of macrophages (M phi), rIL-1, or rIL-2. Resting cloned
HITc cells, purified from residual accessory cells, failed to proliferate in response to FBL alone, but proliferated in response to FBL plus M phi, rIL-1 or rIL-2. Stimulation with FBL alone in the absence of M phi or
IL-1 was sufficient for induction of IL-2R expression, and rendered cells responsive to
IL-2, but M phi or
IL-1 were also required to induce production of
IL-2. The activity of
IL-1 was further examined by measuring the binding of [125I]rIL-1 alpha, which demonstrated that resting cloned
HITc cells expressed IL-1R that increased in number after activation with Ag. This expression of IL-1R and requirement for
IL-1 by CD8+
HITc was surprising because previous studies examining T cell populations after
mitogen stimulation have not detected IL-1R on the CD8+ population. Therefore, the role of
IL-1 in the activation of CD8+ CTL that do not secrete
IL-2 after activation was assessed. By contrast to
HITc, CD8+ CTL required exogenous
IL-2 to proliferate in vitro and did not express IL-1R. These data demonstrate that the subset of CD8+ T cells responsible for
IL-2 production express IL-1R and that triggering this receptor with
IL-1 after Ag stimulation results in the production of
IL-2 and subsequent proliferation.