It has previouslybeen shown that IFN-ais apotent inhibitor of IL-2 induced proliferation in primary T-lymphocytes, by selectively abrogating the downstream e ects of IL-2 on the core cell cycle machinery regulating the G1/S transition. Theoretically this could be mediated through cross-talk between the signalling cascades activated by these cytokines, as several signalling components are known to be shared.