Following infection or vaccination, antigen-specific T cells undergo enormous expansion in numbers and differentiate into effector cells that control infection and modulate other aspects of innate and adaptive immunity. The effector T-cell expansion phase is followed by an abrupt period of contraction, during which 90-95% of antigen-specific T cells are eliminated. The surviving pool of T cells subsequently differentiates into long-lived memory populations that can persist for the life of the host and mediate enhanced protective immunity following pathogen re-infection. The generation and maintenance of memory T-cell populations are influenced by a multitude of factors, including inflammatory cytokines that can act on T cells at various points during their differentiation. Herein, we discuss our current understanding of how inflammation shapes not only the quantity and quality of memory T cells, but also the rate at which functional memory T-cell populations develop.