CD4+ T cell immunity to blood-stage malaria is suboptimal in humans and experimental mice. Two subsets, T-helper 1 (Th1) and follicular helper T cells (Tfh), partially control Plasmodium parasites via IFNγ or by supporting high-affinity antibody production [1]. Discovery of mechanisms controlling Th1/Tfh fate may offer new opportunities for accelerating the onset of immunity to malaria. Previously, we observed early co-expression of chemokine receptors CXCR3 and CXCR5 by Plasmodium-specific TCR transgenic PbTII cells in P.chabaudi-infected mice, prior to their bifurcation towards either Th1 or Tfh fates [2]. We hypothesized here that competition between CXCR3 and CXCR5 influences Th1/Tfh fate in malaria. To test this, genes encoding CXCR3, CXCR5, or CXCR6 were disrupted in naïve PbTIIs via CRISPR/Cas9 and examined for effects on differentiation in vivo. Strikingly, none of these chemokine receptors, either alone or in combination, substantially influenced either PbTII expansion or Th1-differentiation. Instead, by disrupting IL2ra, we determined that early IL-2 signaling, most likely within the first two days of infection, played a critical role in supporting Th1 differentiation, but not clonal expansion. Further experiments suggested IL-2-signalling also controls CD4+ T cell differentiation during experimental vaccination. Hence, the balance between humoral and cellular immunity during malaria infection or vaccination can be modulated by Interleukin-2.