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Sphingosine-1-phosphate (S1P) is a lipid-signaling molecule that regulates numerous biological processes through its interaction with a family of G protein–coupled receptors (S1P1 to S1P5).1 The binding of S1P to the S1P receptor subtype 1 (S1P1), expressed on the surface of lymphocytes, causes the migration of certain types of lymphocytes from lymphoid tissue into the bloodstream. An S1P gradient exists in lymphoid tissues that enables lymphocytes activated in response to antigen recognition to exit lymphoid tissues, enter circulation, migrate to intestinal tissue, and promote inflammation.2-4 S1P signaling does not affect subsets of lymphocytes that do not travel through the lymphoid tissue, and, as a result, these lymphocytes are able to remain in circulation for immune surveillance against infections and tumors.5 Lymphocytes, including B and T cells, play a critical role in regulating pro-inflammatory and anti-inflammatory activity. In inflammatory bowel disease (IBD)—Crohn’s disease and ulcerative colitis—inappropriately activated pro-inflammatory lymphocytes can leave the lymphoid tissue, migrate to the intestines, and promote chronic inflammation.2,4,6 Elevated S1P levels have been linked to IBD, and S1P has been shown to play an important role in the chronic inflammation associated with IBD.2 S1P receptor–targeting agents were successfully used in animal models of IBD. Based on preclinical evidence, targeting the S1P pathway to block S1P gradient–dependent migration of lymphocytes may help reduce chronic inflammation in these diseases.2,4
phosphate in Inflammatory