ENDOGENOUS IL-2 CONTRIBUTES TO T-CELL EXPANSION AND IFN-GAMMA PRODUCTION DURING LYMPHOCYTIC CHORIOMENINGITIS VIRUS-INFECTION

IL-2-deficient mice were used to examine the role of endogenous IL-2 f or supporting T cell proliferative responses during infection with lym phocytic choriomeningitis virus (LCMV). The studies showed that, altho ugh virus-specific CTL activity was induced in the absence of IL-2, th e overall magnitude of the response was profoundly inhibited, Examinat ion of proportions and numbers of CD8(+) T cells demonstrated that the normal virus-induced expansion of these cells was virtually eliminate d in spleens and dramatically decreased in lymph nodes from IL-2-negat ive mice, Absence of endogenous IL-2 also significantly inhibited viru s-induced activated T cell production of IFN-gamma, as well as increas es in frequencies and numbers of IFN-gamma-producing cells, Reductions in immune responses were accompanied by impaired viral clearance, Alt hough T cell responses were dramatically reduced in IL-2-deficient, as compared with IL-2-containing mice, activation signals were being del ivered in vivo because induced CTLs were sensitive to the cell cycle-s pecific toxin, hyduoxyurea (HU), and CD8(+) T cells had induced expres sion of the IL-2R alpha- and beta-chains, These studies demonstrated t hat, although low levels of T cell responses can be induced in the abs ence of IL-2, the factor plays a unique and critical role in supportin g T cell proliferative responses in vivo and in optimizing induction o f the biologic functions mediated by these cells, furthermore, the res ults identify a role for IL-2 in promoting IFN-gamma production in viv o.