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dc.contributor.authorFLETCHER, JEANen
dc.date.accessioned2017-05-25T11:23:25Z
dc.date.available2017-05-25T11:23:25Z
dc.date.issued2016en
dc.date.submitted2016en
dc.identifier.citationBasdeo SA, Kelly S, O?Connell K, Tubridy N, McGuigan C, Fletcher JM, Increased expression of Tbet in CD4+ T cells from clinically isolated syndrome patients at high risk of conversion to clinically definite MS., Springer Plus, 5, 2016, 779-en
dc.identifier.otherYen
dc.identifier.urihttp://hdl.handle.net/2262/80225
dc.descriptionPUBLISHEDen
dc.description.abstractBackground: The ability to identify clinically isolated syndrome (CIS) patients at high risk of progression to clinically definite multiple sclerosis (CDMS) would be clinically beneficial. The initiation of T cell mediated autoimmune diseases such as multiple sclerosis (MS) requires the initial inappropriate activation and differentiation of auto-reactive CD4 + T cells. The quiescence of naive T cells is actively maintained by molecules such as TOB1, which control the threshold of activation. Upon activation, CD4 + T cells can differentiate into various subsets depending on the milieu present. Th1 and Th17 cells are strongly implicated in MS, while regulatory T (Treg) cells constrain autoimmune inflammation and prevent autoimmunity. Findings: We therefore investigated the expression of TOB1, CD44 and Treg, Th1 and Th17 transcription factors in relation to CIS progression. The expression of TOB1 , CD44 , FOXP3 , TBX21 and RORC genes were measured in CD4 + T cells from 10 healthy controls, 20 CIS patients within 3 months of initial clinical presentation and 10 relapsing remit - ting MS patients sampled within 2 months of relapse. CIS patients were subsequently grouped into those who con- verted to CDMS within 1 year and those who remained CIS. No differences in the expression of TOB1 , CD44 , FOXP3 and RORC were observed. There was a significant increase in the expression of the Th1 transcription factor Tbet, encoded by TBX21 , in CIS patients that converted within 1 year compared with those who did not. Conclusion: This pilot data suggests a role for Th1 cells in CIS progression and warrants further evaluation in a larger cohort.en
dc.description.sponsorshipJMF has received honoraria from Novartis and research funding from Abbvie. SB declares that she has no competing interests. CMcG has received research funding from Biogen Idec, Novartis, Bayer and Genzyme and honoraria for advisory boards from Biogen Idec, Novartis and Genzyme. KOC has received travel and educational Grants from Biogen Idec, Novartis, Abvie, Teva and Merck Serono. SK has received financial compensation for travel and presenta- tions given on behalf of Biogen Idec and Novartis. NT has received unre - stricted educational Grants on behalf of the Dept of Neurology at SVUH from Bayer Shering, Biogen, Teva and Novartis.en
dc.format.extent779en
dc.language.isoenen
dc.relation.ispartofseriesSpringer Plusen
dc.relation.ispartofseries5en
dc.rightsYen
dc.subjectClinically isolated syndrome Multiple sclerosis TOB1 T cells Tbeten
dc.subject.lcshClinically isolated syndrome Multiple sclerosis TOB1 T cells Tbeten
dc.titleIncreased expression of Tbet in CD4+ T cells from clinically isolated syndrome patients at high risk of conversion to clinically definite MS.en
dc.typeJournal Articleen
dc.contributor.sponsorScience Foundation Ireland (SFI)en
dc.type.supercollectionscholarly_publicationsen
dc.type.supercollectionrefereed_publicationsen
dc.identifier.peoplefinderurlhttp://people.tcd.ie/fletchjen
dc.identifier.rssinternalid136577en
dc.rights.ecaccessrightsopenAccess
dc.contributor.sponsorGrantNumberBI593en
dc.subject.TCDThemeImmunology, Inflammation & Infectionen
dc.subject.TCDTagAutoimmune Diseases (Multiple Sclerosis, Rheumatoid Arthritis)en
dc.subject.TCDTagMULTIPLE-SCLEROSISen
dc.identifier.rssurihttp://springerplus.springeropen.com/articles/10.1186/s40064-016-2510-0en
dc.identifier.orcid_id0000-0002-0670-6659en
dc.status.accessibleNen


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