NIH VideoCast - Secrets and Lyase: New Roles of S1P Signaling in the Immune System

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Secrets and Lyase: New Roles of S1P Signaling in the Immune System

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Air date:	Wednesday, December 14, 2016, 4:15:00 PM Time displayed is Eastern Time, Washington DC Local
Views:	Total views: 332 (26 Live, 306 On-demand)
Category:	Immunology
Runtime:	00:59:34
Closed captioning:	Check box to display CC outside of the video Note: You can drag the captioning window around and resize it
Description:	Immunology Interest Group Seminar Series Sphingosine 1-phosphate (S1P) signaling plays critical roles in the cardiovascular and immune systems. We have recently characterized a mouse that lacks the S1P transporter SPNS2. SPNS2-deficient mice have only a minor reduction in blood S1P and hence grossly normal vascular permeability, but a dramatic reduction in lymph S1P and hence severely disrupted lymphocyte trafficking. These mice have revealed unexpected functions of S1P gradients in positioning immune cells within lymphoid organs, as well as in supporting lymphocyte survival. Dr. Susan Schwab is Associate Professor at the Skirball Institute of Biomolecular Medicine in New York. She obtained her PhD with Nilabh Shastri at UC Berkeley and she did her post-doctoral fellowship with Jason Cyster at UCSF where she helped define the mechanisms by which the sphingosine 1-phosphate (S1P) receptor regulates lymphocyte egress from lymphoid organs, work that has contributed to now having a S1P lyase inhibitor in clinical trials for treatment of autoimmune disease. In her own lab, Susan has taken on the problem of how S1P gradients are established. Via the generation of a mouse expressing a novel reporter of signaling-available S1P and other elegant tools, her lab has recently identified two new players in the control of S1P distribution: the major facilitator superfamily transporter SPNS2 that facilitates lymphocyte exit from lymph nodes, and lipid phosphate phosphatase 3 which is essential for efficient T cell exit from the thymus and marginal zone B cell shuttling in the spleen. More recently, Susan's lab has found a critical contribution for the chemokine receptor CXCR4 in disease progression of T cell acute lymphoblastic leukemia (T-ALL) in both mouse and human xenograft models of the disease, a finding with potential important translational implications.

NLM Title:	Secrets and lyase : new roles of S1P signaling in the immune system / Susan Schwab.
Author:	Schwab, Susan. National Institutes of Health (U.S.),
Publisher:
Abstract:	(CIT): Sphingosine 1-phosphate (S1P) signaling plays critical roles in the cardiovascular and immune systems. We have recently characterized a mouse that lacks the S1P transporter SPNS2. SPNS2-deficient mice have only a minor reduction in blood S1P and hence grossly normal vascular permeability, but a dramatic reduction in lymph S1P and hence severely disrupted lymphocyte trafficking. These mice have revealed unexpected functions of S1P gradients in positioning immune cells within lymphoid organs, as well as in supporting lymphocyte survival. Dr. Susan Schwab is Associate Professor at the Skirball Institute of Biomolecular Medicine in New York. She obtained her PhD with Nilabh Shastri at UC Berkeley and she did her post-doctoral fellowship with Jason Cyster at UCSF where she helped define the mechanisms by which the sphingosine 1-phosphate (S1P) receptor regulates lymphocyte egress from lymphoid organs, work that has contributed to now having a S1P lyase inhibitor in clinical trials for treatment of autoimmune disease. In her own lab, Susan has taken on the problem of how S1P gradients are established. Via the generation of a mouse expressing a novel reporter of signaling-available S1P and other elegant tools, her lab has recently identified two new players in the control of S1P distribution: the major facilitator superfamily transporter SPNS2 that facilitates lymphocyte exit from lymph nodes, and lipid phosphate phosphatase 3 which is essential for efficient T cell exit from the thymus and marginal zone B cell shuttling in the spleen. More recently, Susan's lab has found a critical contribution for the chemokine receptor CXCR4 in disease progression of T cell acute lymphoblastic leukemia (T-ALL) in both mouse and human xenograft models of the disease, a finding with potential important translational implications.
Subjects:	Receptors, Lysosphingolipid--immunology Signal Transduction--immunology
Publication Types:	Lecture Webcast

NLM Classification:	QU 55.7
NLM ID:	101698570
CIT Live ID:	18538
Permanent link:	https://videocast.nih.gov/watch=18538

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