In the absence of the cytokine IL-27 , infection with the parasite leads to the development of a T cell mediated hyper-inflammatory response dominated by the production of IFN-g. Previous studies indicate that some of the suppressive effects are associated with the ability to inhibit the production of IL-2 and IL-17 while at the same time it promotes the expression of inhibitory pathways mediated through IL-10 and inhibitory receptors. However, the precise role of IL-27 in control of pathogen specific and potentially pathogenic T cell responses is not well understood. In the present studies we assessed the impact of IL-27 on the transition of T cell subtypes (based on expression of CXCR3 and KLRG1) and expression of effector cytokines. These studies indicate that IL-27 restrains the differentiation of the terminal effector T cells from proliferative intermediates and thus restricts the production of effector cytokines from parasite-specific T cells.