Defective sphingosine 1-phosphate receptor 1 (S1P1) phosphorylation exacerbates TH17-mediated autoimmune neuroinflammation View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2013-11

AUTHORS

Christopher S Garris, Linfeng Wu, Swati Acharya, Ahmet Arac, Victoria A Blaho, Yingxiang Huang, Byoung San Moon, Robert C Axtell, Peggy P Ho, Gary K Steinberg, David B Lewis, Raymond A Sobel, David K Han, Lawrence Steinman, Michael P Snyder, Timothy Hla, May H Han

ABSTRACT

Sphingosine 1-phosphate (S1P) signaling regulates lymphocyte egress from lymphoid organs into systemic circulation. The sphingosine phosphate receptor 1 (S1P1) agonist FTY-720 (Gilenya) arrests immune trafficking and prevents multiple sclerosis (MS) relapses. However, alternative mechanisms of S1P-S1P1 signaling have been reported. Phosphoproteomic analysis of MS brain lesions revealed S1P1 phosphorylation on S351, a residue crucial for receptor internalization. Mutant mice harboring an S1pr1 gene encoding phosphorylation-deficient receptors (S1P1(S5A)) developed severe experimental autoimmune encephalomyelitis (EAE) due to autoimmunity mediated by interleukin 17 (IL-17)-producing helper T cells (TH17 cells) in the peripheral immune and nervous system. S1P1 directly activated the Jak-STAT3 signal-transduction pathway via IL-6. Impaired S1P1 phosphorylation enhances TH17 polarization and exacerbates autoimmune neuroinflammation. These mechanisms may be pathogenic in MS. More... »

PAGES

1166-1172

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ni.2730

DOI

http://dx.doi.org/10.1038/ni.2730

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1044553169

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/24076635


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