Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis (TB), is the leading cause of mortality due to a single infectious organism. While generally curable, TB requires a lengthy and complex antibiotic regimen, due in large part to persistent bacteria that survive antibiotic exposure. Rel is the primary enzyme regulating the stringent response, which contributes to Mtb persistence. Targeting Rel with a vaccine to eliminate persistent bacteria in combination with antibiotics to kill dividing bacteria has shown promise in model systems. In a mouse model of Mtb infection, a vaccine created by genetically fusing rel to the chemokine macrophage inflammatory protein 3α (MIP3α), a ligand for the CC chemokine receptor type 6 (CCR6) present on immature dendritic cells, has been shown to enhance T-cell responses and accelerate eradication of infection in mouse models compared to a vaccine lacking the chemokine component. In this study, immunogenicity studies in the mouse and rhesus macaque models provide evidence that intranasal administrations of the DNA form of the MipRel vaccine led to enhanced lung infiltration of T cells after a series of immunizations. Furthermore, despite similar systemic T-cell responses following MipRel or Rel vaccination, lung and bronchoalveolar lavage cell samples were more enriched for cytokine-secreting T cells in MipRel groups compared to Rel groups. We conclude that intranasal immunization with a simple MIP-3α fusion DNA vaccine represents a novel strategy for eliciting T-cell immune responses to antigens of interest within the respiratory tract. That this formulation is immunogenic in a non-human primate model historically viewed as poorly responsive to DNA vaccines indicates the potential for clinical application in the treatment of Mtb infection, with possible applications to other respiratory pathogens.