This dissertation shows that the ancient Wnt and Notch signaling modules have been coopted by the immune system to direct T-cell responses. Notch has turned out to be particularly dedicated to induction of effector cell differentiation and function. Lack of Notch activation may predispose cells to less terminally differentiated fates, as most prominently suggested by our results on CD8+ T-cells. A more restricted role seems to be played by Wnt, which selectively controls survival of a subset of effector cells. With these studies, we have identified some of the cogwheels and springs that control the inner workings of the immune system.