{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Lee LF"],"funding":["NINDS NIH HHS"],"pagination":["93ra68"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3739690"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["3(93)"],"pubmed_abstract":["The interleukin-7 receptor α chain (IL-7Rα) gene was identified as a top non-major histocompatibility complex-linked risk locus for multiple sclerosis (MS). Recently, we showed that a T helper 1 (T(H)1)-driven, but not a T(H)17-driven, form of MS exhibited a good clinical response to interferon-β (IFN-β) therapy. We now demonstrate that high serum levels of IL-7, particularly when paired with low levels of IL-17F, predict responsiveness to IFN-β and hence a T(H)1-driven subtype of MS. We also show that although IL-7 signaling is neither necessary nor sufficient for the induction or expansion of T(H)17 cells, IL-7 can greatly enhance both human and mouse T(H)1 cell differentiation. IL-7 alone is sufficient to induce human T(H)1 differentiation in the absence of IL-12 or other cytokines. Fur"],"journal":["Science translational medicine"],"pubmed_title":["IL-7 promotes T(H)1 development and serum IL-7 predicts clinical response to interferon-β in multiple sclerosis."],"pmcid":["PMC3739690"],"funding_grant_id":["R01NS 55997","K99 NS075099","1K99NS075099-01","R01 NS055997"],"pubmed_authors":["Lee LF","Lin JC","Steinman L","Killestein J","Dilley J","de Jong BA","Walker MG","Yu J","Evering W","Han B","Tu GH","Axtell R","Polman CH","Logronio K","Shi J","Rickert M"],"additional_accession":[]},"is_claimable":false,"name":"IL-7 promotes T(H)1 development and serum IL-7 predicts clinical response to interferon-β in multiple sclerosis.","description":"The interleukin-7 receptor α chain (IL-7Rα) gene was identified as a top non-major histocompatibility complex-linked risk locus for multiple sclerosis (MS). Recently, we showed that a T helper 1 (T(H)1)-driven, but not a T(H)17-driven, form of MS exhibited a good clinical response to interferon-β (IFN-β) therapy. We now demonstrate that high serum levels of IL-7, particularly when paired with low levels of IL-17F, predict responsiveness to IFN-β and hence a T(H)1-driven subtype of MS. We also show that although IL-7 signaling is neither necessary nor sufficient for the induction or expansion of T(H)17 cells, IL-7 can greatly enhance both human and mouse T(H)1 cell differentiation. IL-7 alone is sufficient to induce human T(H)1 differentiation in the absence of IL-12 or other cytokines. Fur","dates":{"release":"2011-01-01T00:00:00Z","publication":"2011 Jul","modification":"2025-04-04T21:09:35.45Z","creation":"2019-03-27T01:14:23Z"},"accession":"S-EPMC3739690","cross_references":{"pubmed":["21795588"],"doi":["10.1126/scitranslmed.3002400"]}}