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

View areas of research related to S1PR


  1. Bamias G, Clark DJ, Rivera-Nieves J. Curr Drug Targets. 2013;14(12):1490-1500.
  2. Brinkmann V, Billich A, Baumruker T, et al. Nat Rev Drug Discov. 2010;9(11):883-897.
  3. Pham THM, Okada T, Matloubian M, et al. Immunity. 2008;28(1):122-133.