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- W2948265378 abstract "Abstract Group 3 Innate lymphoid cells (ILC3) resemble to Th17 cells in their production of effector cytokines and tissue localization. Th17 cells have been shown to be pathogenic in mouse MS models. Previous studies from others and our lab have shown that Sphingosine 1 phosphate 1 (S1P1) receptor impacts Th17 cell biology. S1P1 receptor agonist Fingolimod is used in the treatment of Multiple sclerosis (MS). To this day, however, the effects of fingolimod on human ILC populations have not been studied. In this study, using PBMCs from Fingolimod-receiving or control relapsing-remitting MS patients, combined with ex vivo culture system we characterized the impact of S1P1 agonists on ILC populations via Flow cytometry, real-time qPCR and ELISA. We report that human ILCs express S1P1 receptor, respond to it, as evident in reduced peripheral ILC cellularity in MS patients receiving Fingolimod. Also in culture, exposure to S1P1 agonists reduced gene expression and secretion of GMCSF and IFN-g by human ILC3 and ILC1, respectively. To our knowledge, this is the first report to study the impact of fingolimod on ILC populations in MS patients." @default.
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- W2948265378 date "2018-05-01" @default.
- W2948265378 modified "2023-09-26" @default.
- W2948265378 title "Fingolimod impacts innate lymphoid cell biology" @default.
- W2948265378 doi "https://doi.org/10.4049/jimmunol.200.supp.41.10" @default.
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