<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Lee LF</submitter><funding>NINDS NIH HHS</funding><pagination>93ra68</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3739690</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>3(93)</volume><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</pubmed_abstract><journal>Science translational medicine</journal><pubmed_title>IL-7 promotes T(H)1 development and serum IL-7 predicts clinical response to interferon-β in multiple sclerosis.</pubmed_title><pmcid>PMC3739690</pmcid><funding_grant_id>R01NS 55997</funding_grant_id><funding_grant_id>K99 NS075099</funding_grant_id><funding_grant_id>1K99NS075099-01</funding_grant_id><funding_grant_id>R01 NS055997</funding_grant_id><pubmed_authors>Lee LF</pubmed_authors><pubmed_authors>Lin JC</pubmed_authors><pubmed_authors>Steinman L</pubmed_authors><pubmed_authors>Killestein J</pubmed_authors><pubmed_authors>Dilley J</pubmed_authors><pubmed_authors>de Jong BA</pubmed_authors><pubmed_authors>Walker MG</pubmed_authors><pubmed_authors>Yu J</pubmed_authors><pubmed_authors>Evering W</pubmed_authors><pubmed_authors>Han B</pubmed_authors><pubmed_authors>Tu GH</pubmed_authors><pubmed_authors>Axtell R</pubmed_authors><pubmed_authors>Polman CH</pubmed_authors><pubmed_authors>Logronio K</pubmed_authors><pubmed_authors>Shi J</pubmed_authors><pubmed_authors>Rickert M</pubmed_authors></additional><is_claimable>false</is_claimable><name>IL-7 promotes T(H)1 development and serum IL-7 predicts clinical response to interferon-β in multiple sclerosis.</name><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</description><dates><release>2011-01-01T00:00:00Z</release><publication>2011 Jul</publication><modification>2025-04-04T21:09:35.45Z</modification><creation>2019-03-27T01:14:23Z</creation></dates><accession>S-EPMC3739690</accession><cross_references><pubmed>21795588</pubmed><doi>10.1126/scitranslmed.3002400</doi></cross_references></HashMap>