Immunotherapeutic drugs that mimic sphingosine 1-phosphate (S1P) disrupt lymphocyte
trafficking and cause T helper and T effector cells to be retained in secondary lymphoid
tissue and away from sites of inflammation. The prototypical therapeutic agent, 2-alkyl-2-
amino-1, 3-propanediol (FTY720), stimulates S1P signaling pathways only after it is
phosphorylated by one or more unknown kinases. We generated sphingosine kinase 2
(SPHK2) null mice to demonstrate that this kinase is responsible for FTY720 …