Journal
RHEUMATOLOGY
Volume 53, Issue 9, Pages 1560-1569Publisher
OXFORD UNIV PRESS
DOI: 10.1093/rheumatology/ket414
Keywords
biologic; Th17 cell; IL-17; IL-17A; IL-12; IL-23; rheumatoid arthritis; autoimmune disease; inflammation; synovitis
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Funding
- Novartis Pharma AG, Basel, Switzerland
- Cancer Research UK
- Versus Arthritis [18475] Funding Source: researchfish
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Biologic therapies that target pathogenic cytokines such as TNF, IL-1 beta or IL-6 have greatly improved the treatment of RA. Unfortunately, not all RA patients respond to current biologic therapies and responses are not always maintained, suggesting that there are alternative drivers of RA pathogenesis that might serve as promising therapeutic targets. Discovery of the new Th17 subset of Th cells, and their role in autoimmune disease development, has implicated the proinflammatory IL-12 and IL-17 families of cytokines in RA disease pathogenesis. Members of these cytokine families are elevated in the blood and joints of RA patients and have been shown to remain elevated in patients who do not respond to current biologics. In addition, these cytokines have been shown to play roles in joint destruction and erosion. A new subclass of biologics that target the IL-12 and/or IL-17 signalling pathways are under development. Here we review evidence for a role of Th17 cells as well as IL-12 and IL-17 cytokines in RA pathogenesis as the rationale for a subsequent discussion of the ongoing and completed clinical trials of newly emerging biologic therapies directed at IL-12 or IL-17 pathway inhibition.
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