The ability of T cells to recirculate from lymph nodes to the blood and then into tissues is essential for the perpetuation of chronic inflammatory processes.¹

• Circulation of T cell subsets (naïve and central memory T cells) between lymph nodes and blood is mediated by two opposing receptors: Sphingosine 1-Phosphate Receptor Type 1 (S1P-1R) favors T cell egress while CC-chemokine receptor type 7 (CCR7) favors retention in the node.^2,3
• To egress from lymph nodes, the T cells require activation of S1P-1R by endothelial cell-generated S1P. S1P-1R activation overrides the lymph node retention effect of CCR7.²
• Targeted modulation of S1P-1R causes aberrant internalization of the receptor and reduces the responsiveness of T cells to the S1P egress signal, favoring T cell retention in the lymph nodes.²