Lymphoid tissue chemokines limit priming duration to preserve CD8 + T cell functionality

The generation of effector CD8 + T cells (T EFF ) requires activation of naïve CCR7 + T cells (T N ) by dendritic cells (DCs) in lymphoid tissue. How T N -DC interaction duration and signal integration are controlled remains unclear. In this study, we show that lymphoid stroma–secreted CCR7 ligands limit interaction duration by progressively inducing CD8 + T cell release from DCs. At late interaction stages, CCR7 ligands relocalize the F-actin regulator DOCK2 away from the DC interface, permitting T cell detachment, proliferation onset, and acquisition of cytotoxicity. Disruption of CCR7 signaling causes prolonged T cell–DC contacts and produces dysfunctional T EFF with elevated inhibitory receptors, reduced antimicrobial activity, and impaired recall responses. Stromal chemokines therefore act as critical regulators of T cell priming by DCs, preserving CD8 + effector function during acute and memory phases.