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The rationale for Janus kinase inhibitors for the treatment of spondyloarthritis.
Veale, Douglas J McGonagle, Dennis McInnes, Iain B Krueger, James G Ritchlin, Christopher T Elewaut, Dirk Kanik, Keith S Hendrikx, Thijs Berstein, Gabriel Hodge, Jennifer
Veale, Douglas J
McGonagle, Dennis
McInnes, Iain B
Krueger, James G
Ritchlin, Christopher T
Elewaut, Dirk
Kanik, Keith S
Hendrikx, Thijs
Berstein, Gabriel
Hodge, Jennifer
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Keywords
ARTHRITIS
IMMUNOLOGY
INFLAMMATORY DISEASES
RHEUMATOLOGY
IMMUNOLOGY
INFLAMMATORY DISEASES
RHEUMATOLOGY
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key070.pdf
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Abstract
The 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.
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en
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ISSN
eISSN
1462-0332
ISBN
DOI
10.1093/rheumatology/key070
PMID
29618084