CD8 T cells have largely been thought to only play a role during the liver stages of Plasmodium infection. Recent work, however, has demonstrated that CD8 T cells can recognized and kill P. vivax-infected reticulocytes as these cells retain MHC-I expression. This has opened an exciting new field for Pv immunology and vaccinology, and yet the limitations on accessing both Pv parasites and relevant immune cells from infected persons slows the mechanistic work needed to chart a path forward for T cell-based vaccines targeting the blood stages. Here, we use P. cynomolgi infection of rhesus macaques to show that the CD8 T cell killing of infected reticulocytes is conserved in this animal model. In addition, at least 48/50 MHC-I-presented epitopes that are recognized by CD8 T cells during natural Pv infection are also recognized by CD8 T cells from Pc-infected rhesus macaques. Finally, MHC restriction analysis demonstrated that CD8 T cell responses to 7 of the 9 epitopes tested are restricted to MHC-E, the highly conserved MHC class I molecule, in Pc-infected rhesus macaques. Further analysis of the role of MHC-E antigen presentation in T cell killing of infected reticulocytes is underway. Together, these results further demonstrate the utility of the Pc animal model for Pv immunoparasitology research and that it can be used to discover and validate novel T cell immune mechanisms. Given the extreme conservation of MHC-E across all primates, this also paves the way for the development of malaria vaccines that are not susceptible to HLA/MHC polymorphisms if they are designed to be based on MHC-E presentation. Importantly, our work demonstrates that this can be done in a human-relevant animal model that simultaneously allows iterative vaccination-challenge studies alongside mechanistic studies of immune mechanisms not feasible using human studies alone.