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dc.contributor.authorVeale, Douglas J
dc.contributor.authorMcGonagle, Dennis
dc.contributor.authorMcInnes, Iain B
dc.contributor.authorKrueger, James G
dc.contributor.authorRitchlin, Christopher T
dc.contributor.authorElewaut, Dirk
dc.contributor.authorKanik, Keith S
dc.contributor.authorHendrikx, Thijs
dc.contributor.authorBerstein, Gabriel
dc.contributor.authorHodge, Jennifer
dc.contributor.authorTelliez, Jean-Baptiste
dc.date.accessioned2020-01-30T16:59:11Z
dc.date.available2020-01-30T16:59:11Z
dc.identifier.pmid29618084
dc.identifier.doi10.1093/rheumatology/key070
dc.identifier.urihttp://hdl.handle.net/10147/627108
dc.description.abstractThe pathogenesis of SpA is multifactorial and involves a range of immune cell types and cytokines, many of which utilize Janus kinase (JAK) pathways for signaling. In this review, we summarize the animal and pre-clinical data that have demonstrated the effects of JAK blockade on the underlying molecular mechanisms of SpA and provide a rationale for JAK inhibition for the treatment of SpA. We also review the available clinical trial data evaluating JAK inhibitors tofacitinib, baricitinib, peficitinib, filgotinib and upadacitinib in PsA, AS and related inflammatory diseases, which have demonstrated the efficacy of these agents across a range of SpA-associated disease manifestations. The available clinical trial data, supported by pre-clinical animal model studies demonstrate that JAK inhibition is a promising therapeutic strategy for the treatment of SpA and may offer the potential for improvements in multiple articular and extra-articular disease manifestations of PsA and AS.en_US
dc.language.isoenen_US
dc.subjectARTHRITISen_US
dc.subjectIMMUNOLOGYen_US
dc.subjectINFLAMMATORY DISEASESen_US
dc.subjectRHEUMATOLOGYen_US
dc.titleThe rationale for Janus kinase inhibitors for the treatment of spondyloarthritis.en_US
dc.typeArticleen_US
dc.identifier.eissn1462-0332
dc.identifier.journalRheumatology (Oxford, England)en_US
dc.description.provinceLeinsteren_US
dc.description.peer-reviewpeer-reviewen_US
dc.source.journaltitleRheumatology (Oxford, England)
dc.source.volume58
dc.source.issue2
dc.source.beginpage197
dc.source.endpage205
refterms.dateFOA2020-01-30T16:59:11Z
dc.source.countryEngland


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