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. Author manuscript; available in PMC: 2012 Jun 6.
Published in final edited form as: Nat Rev Immunol. 2011 May 6;11(6):403–415. doi: 10.1038/nri2974

Figure 2. Regulation of T cell egress by S1PR1.

Figure 2

When mature single-positive (SP) thymocytes are ready to exit the thymus (a), they upregulate Krüppel-like factor 2 (KLF2) and its target sphingosine-1-phosphate receptor 1 (S1PR1). The re-expression of S1PR1 enables thymocytes to exit the thymus in response to S1P locally supplied by perivascular cells before encountering the endothelium and then the high levels of S1P in blood vessels. S1PR1 on circulating T cells is internalized owing to high levels of S1P and reappears when the T cells enter non-inflamed lymphoid tissues (b) that contain low levels of S1P. However, in inflamed lymphoid tissues (c), CD69 is expressed on lymphocytes and causes internalization and degradation of S1PR1 to delay exit. After undergoing several rounds of division, the newly generated effector T cells upregulate S1PR1, lose CC-chemokine receptor 7 (CCR7) expression and exit into the circulation. TCR, T cell receptor.