Suzanne M. Mandala

TL;DR: It is shown that lymphocyte trafficking is altered by the lysophospholipid sphingosine-1-phosphate (S1P) and by a phosphoryl metabolites of the immunosuppressive agent FTY720.

TL;DR: Gas chromatography and gas chromatography/mass spectroscopy analyses reveal that null mutations of ELO2and ELO3 produce defects in the formation of very long chain fatty acids, indicating that these genes encode components of the membrane-bound fatty acid elongation systems that produce the 26-carbon very longChain fatty acids that are precursors for ceramide and sphingolipids.

TL;DR: The results with these Sphk1 null mice reveal that some key physiologic processes that require S1P receptor signaling, such as vascular development and proper lymphocyte distribution, can occur in the absence of SPHK1.

TL;DR: The results indicated that the expression of the S1P1 receptor on T-cells controls their exit from the thymus and entry into the blood and, thus, has a central role in regulating the numbers of peripheral T- cells.

TL;DR: Three lines of evidence link S1P3 receptor activity with acute toxicity and cardiovascular regulation: compound potency on S 1P3 correlated with toxicity and bradycardia; the shift in potency of phosphorylated-FTY720 for inducing lymphopenia versus brady Cardia and hypertension was consistent with affinity for S1 p1 relative to S1p3; and toxicity, brady cardia, and hypertension were absent in S1 P3-/- mice.