The timing and location of the interferon (IFN) response to viral infection is tightly coordinated. High expression or therapeutic administration of type-I IFN (IFN-I) enhances viral clearance, whereas deficiency or blocking of IFN-I prolongs infection. We have previously shown that deficiency in the IFN-I receptor, IFNAR promotes the formation of CD8+ T cell stem like memory cells (Tscm) due to cellular retention in the T cell paracortex where this fate is imprinted. This highlights the tension between effector and Tscm fates that can be leveraged by increasing IFN-I or blocking IFNAR. Here, we demonstrate that blocking IFNAR precisely at the start of LCMV infection results in potent Tscm formation, but unintuitively increases the levels of CXCR3 ligands. This suggests the mechanism of retention in the T cell paracortex, is due increased chemokine abundance and desensitization of CXCR3. Blocking IFNAR increased the recruitment of monocyte-derived inflammatory DCs in an IFNg-dependent fashion. In the absence of both IFNAR and IFNg chemokine expression was lost. In this setting Tscm fate was still enhanced and occurred along-side T cell exhaustion and persistent viral load. This study reveals the interplay of IFN-I and IFN-II that can be harnessed during vaccination to induce potent stem-like memory.