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• W2023962954 abstract "Sphingosine 1-phosphate (S1P) and 5 specific high-affinity S1P receptor (S1PR) subtypes, S1P_1–5, have important regulatory functions in normal physiology and disease processes, particularly involving the immune, central nervous, and cardiovascular systems. Within the immune system, downmodulation of S1P₁ prevents the egress of B and T cells from lymph nodes (LN) into the lymphatic circulation. This is especially relevant in certain autoimmune diseases, including multiple sclerosis (MS), in which demyelination and brain atrophy occur due to the presence of autoreactive lymphocytes within the CNS. Accordingly, S1P₁-directed pharmacologic interventions that aim to retain these autoreactive lymphocytes in the LN and thus prevent their recirculation and subsequent infiltration into the CNS have been investigated as a means of preventing disease progression in patients with MS. Fingolimod (FTY720), a structural analog of sphingosine, is phosphorylated in vivo into fingolimod phosphate by sphingosine kinase-2. Fingolimod phosphate, which binds to S1PRs, has been shown to modulate the activity of S1P₁ in patients with MS and to reduce immune cell infiltration into the CNS, consistent with its previously established effects in animal models of the disease. Preclinical studies also suggest that fingolimod has beneficial effects within the CNS that are independent of its immune cell trafficking activity. This review highlights the normal physiologic processes modulated by S1P and S1PRs, and the therapeutic effects of S1PR modulation in the immune, central nervous, and cardiovascular systems." @default.
• W2023962954 created "2016-06-24" @default.
• W2023962954 creator A5006724562 @default.
• W2023962954 creator A5080557819 @default.
• W2023962954 date "2011-02-21" @default.
• W2023962954 modified "2023-10-11" @default.
• W2023962954 title "Sphingosine 1-phosphate (S1P): Physiology and the effects of S1P receptor modulation" @default.
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• W2023962954 doi "https://doi.org/10.1212/wnl.0b013e31820d5ec1" @default.
• W2023962954 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21339489" @default.
• W2023962954 hasPublicationYear "2011" @default.
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