Repeated Plasmodium falciparum infections drive the development of clinical immunity to human malaria. However, immunological mechanisms underpinning this response are only partially understood. γδ T cells have been linked to clinical protection from malaria, but how adaptive-like Vδ1+ T cells respond to repeated P. falciparum infections is unclear. We investigated the impact of repeated P. falciparum infections on γδ T cell subsets and the γδ T cell receptor (TCR) repertoire in humans. We studied peripheral blood samples from Australian children, Malian children naturally exposed to malaria, and U.S. adults serially challenged with four repeated controlled human malaria infections (CHMIs). Clonally expanded cytotoxic Vδ1effector T cells were a major component of the γδ T cell compartment in Malian children compared to malaria-naïve Australian children. Sequential CHMIs initiated a robust innate-like Vδ2+ T cell response to three P. falciparum infections in malaria-naïve U.S. adults, however, these cell frequencies declined between infections and were not sustained after the fourth infection. In contrast, Vδ1+ T cell frequencies increased after repeated infection and correlated with clinical immunity to malaria. Populations of Vδ1naive T cells differentiated into cytotoxic Vδ1effector cells concomitant with waves of clonal selection after each infection. Finally, Vδ1+ T cells from individuals with a history of malaria were licensed for in vitro P. falciparum parasite reactivity. Together, our study indicates that repeated P. falciparum infections drive the clonal expansion of an adaptive γδ T cell repertoire and establishes a role for Vδ1+ T cells in the human immune response to malaria.