The ultraviolet (UV) component of sunlight is a major contributor to skin cancer development. However multiple epidemiological and empirical studies have highlighted the protective effect of UV from multiple sclerosis. How UV protects from CNS-autoimmunity is not well understood. Studies in mice have revealed an important role for UV-induced immune suppression, in part via the activation of regulatory B cells. UV manipulation of normal lymphocyte recirculation by “trapping” them in skin-draining lymph nodes may be another important mechanism. We hypothesised that UV was sequestering lymphocytes within lymph nodes by altering sphingosine-1-phosphate (S1P), a lipid chemoattractant critical to the recirculation of lymphocytes. C57BL/6 mice were exposed, or not, to a single dose of solar simulated UV irradiation. 24 hours later, lymph node and plasma lipids were extracted and quantified by liquid chromatography tandem-mass spectrometry. UV exposure significantly increased S1P levels within skin-draining lymph nodes. Flow cytometry analysis highlighted that this corresponded to a decrease in cell-surface expression of the S1P receptor, S1P₁, indicating an inhibition of cell egress. Although plasma S1P was unaffected, exposure to UV decreased the numbers of naïve and effector memory T cells in peripheral blood with a concomitant increase in skin-draining lymph nodes. S1P production in the skin-draining lymph nodes was unchanged indicating that UV may be facilitating lymphocyte trapping by preventing the degradation of S1P. These results show that UV manipulates the S1P pathway which may explain the lymphocyte sequestration in the skin-draining lymph nodes, and the subsequent protection from CNS-targeted autoimmunity.