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Article Summary
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Gerlinde LS et al. – Activation of the interleukin-23/interleukin-17 axis in spondyloarthritis has important therapeutic implications. Methods- A review to (i) inform readers of recent advances in our understanding of the development and function of Th17 T cells and (ii) emerging data suggesting that the IL-23/IL-17 axis may be involved in the pathogenesis of spondyloarthritis
Results- The discovery of CD4+ Th17 T cells and the IL-23/IL-17 axis has challenged existing paradigms and the role of Th1 T cells in many autoimmune diseases
- In humans, IL-23 synergizes with IL-6 and IL-1 to promote Th17 development
- In mice, TGF-β and IL-6 are critical, whereas IL-23 is more important at later stages promoting IL-17 production
- In mice, CD4+ cells producing IF-γ appear to be distinct from IL-17-producing cells, while in humans cells secreting both cytokines have been observed
- Growing evidence suggest that the IL-23/IL-17 axis plays an important role in spondyloarthritis pathogenesis
- Possible links between an HLA-B27-induced unfolded protein response and activation of the IL-23/IL-17 axis may contribute to the development of the spondyloarthritis phenotype
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