Abstract
Abstract Sphingosine 1-phosphate (S1P) in blood and lymph controls lymphoid traffic and tissue migration of T cells through signals from the type 1 S1P receptor (S1P1), but less is known of effects of the S1P-S1P1 axis on non-migration functions of T cells. CD4 T cells from a double transgenic (DTG) mouse express OTII TCRs specific for ovalbumin peptide 323–339 (OVA) and a high level of TG S1P1, resistant to suppression by T cell activation. Activated DTG CD4 T cells respond as expected to S1P by chemotactic migration and reduction of OVA-evoked secretion of IFN-gamma. In addition, DTG CD4 T cells stimulated by OVA secrete a mean of 2.5-fold more IL-17 than those from OTII single TG mice with concomitantly higher levels of mRNA encoding IL-17 by real-time PCR and intracellular IL-17 detected by ELISpot assays. OVA challenge of subcutaneous air-pockets elicited influx of more OTII-TCR-positive T cells producing a higher level of IL-17 in DTG mice than OTII control mice. Augmentation of the number and activity of Th17 cells by the S1P-S1P1 axis may enhance host defense against microbes and in other settings increase host susceptibility to autoimmune diseases. (supported by NIH HL31809)
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