Memory CD8⁺ T cells are important for controlling reinfection against intracellular pathogens, yet the migratory signals required for CD8⁺ T cell memory formation are poorly understood. In this study, we show that the chemokine receptor CCR2 is expressed on CD8⁺ T cells following influenza A infection. CCR2-deficient antigen-specific CD8⁺ T cells displayed normal effector cell differentiation and cytokine production but impaired development of memory precursor cells. Furthermore, CCR2^-/- CD8⁺ T cells had reduced proliferation in the late stages of infection. This led to enhanced CD8⁺ T cell contraction alongside a cell intrinsic defect in the formation of central and tissue-resident memory CD8⁺ T cells. Consistent with these observations, CCR2^-/- memory CD8⁺ T cells failed to efficiently control secondary infection against intracellular pathogens. These data uncover a novel CCR2-dependent pathway critical for generating memory CD8⁺ T cells.