Experimental infection with the intracellular protozoan Leishmania major conн stitutes a particularly versatile model for assessing the role of CD4+ subset deн velopment in the host response to infectious disease. The association of Thl development with control of infection, and of Th2 cell development with proн gressive disease, has been well established. The capacity to manipulate the outн come, using distinct immunologic interventions, in both genetically resistant and susceptible mice has identified key effector cytokines that must be present during the time of initial priming of T cells in order to affect the CD4 switch phenotype.