Lymphoid tissue chemokines limit priming duration to preserve CD8(+) T cell functionality
Summary
The generation of effector CD8+ T cells (TEFF) requires activation of naïve CCR7+ T cells (TN) by dendritic cells (DCs) in lymphoid tissue. How TN-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
Content
# Lymphoid tissue chemokines limit priming duration to preserve CD8(+) T cell functionality
*Published: 2026 Apr 30*
The generation of effector CD8+ T cells (TEFF) requires activation of naïve
CCR7+ T cells (TN) by dendritic cells (DCs) in lymphoid tissue. How TN-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 TEFF 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.
DOI: 10.1126/science.adq2080