infection. Next, we performed adoptive transfer assays to determine if IL17RA expression on the CTL itself provided an advantage to survive and respond to Tc. First, we transferred CTL from CD45.1 WT mice into CD45.2 WT and KO host and analyzed upon infection, the contribution of the injected cells to the CTL response. After 20 days post infection (dpi), the contribution of injected CD45.1 CTL to Tc-specific CTL pools was higher in KO than in WT hosts (blood p=0.003; spleen p=0.011). Convincingly, we transferred equal numbers of CTL from CD45.1 WT and CD45.2 KO mice into CD45.1/2 hosts. After 20dpi, injected KO CTL
were significantly outcompeted by their WT counterparts (blood p=0.016; spleen p=0.014). To elucidate the IL17 cytokine critical for CTL responses, we evaluated how lack of IL17A/F affected the course of Tc infection. Infected IL17A/F KO mice showed the same phenotype than infected KO mice (i.e. increased tissue parasitism, reduced total and Tc-specific CTL and exhausted CTL phenotype). Finally, we determined that purified naive CTL upregulated IL17RA expression upon TCR engagement and become responsive to rIL17A that diminished the % of AnnexinV+ cells (p<0.01). We conclude that IL17A/F promote robust CTL responses<