Malaria infection still remains one of the world’s most formidable issues across both health and economical systems. Despite the best intervention strategies over 200 million people are infected with malaria annually, and mortality rates exceed 400,000 deaths per year. In order to develop effective therapeutics and vaccines a better understanding of fundamental human immunology is required. This is particularly true of the contribution of T cells to malaria defence. Research to date comes from field samples which can sometimes be difficult to interpret due to confounding factors including multiple exposures. As such, the underlying immune correlates of an efficient response remain unknown. To investigate the role of T cells in disease we used a human model of blood stage Plasmodium falciparum infection involving the Medicines for Malaria Venture (MMV). Using NanoString profiling, we performed high-dimensional phenotyping of T cell subsets before infection, during infection and during convalescence. Plasmodium falciparum infection resulted in marked phenotypic ‘scaring’ across all T cell subsets. This distinct phenotype persisted during convalescence. We also identified gene modules that correlated with parasitaemia revealing a possible continua between individuals at risk of disease and ‘elite controllers’. These T cell genes may serve as novel proxies of disease burden and/or assist in identifying pathways for immunotherapies or vaccine activation. Indeed, characterising the T cell biology of elite controllers opens the possibility of inducing this phenotype for the purposes of rational vaccine design and therapeutic intervention.