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Effects of the IL-23-IL-17 pathway on bone in spondyloarthritis.
- Source :
-
Nature Reviews Rheumatology . Nov2018, Vol. 14 Issue 11, p631-640. 10p. - Publication Year :
- 2018
-
Abstract
- Over the past several years, a pathophysiological role for the IL-23-IL-17 pathway in human disease has been defined. A subset of rheumatic diseases, including psoriatic arthritis (PsA) and ankylosing spondylitis (AS), are now acknowledged to be triggered by dysregulated IL-23-IL-17 pathway activation. Genetic evidence links the IL-23-IL-17 pathway to inflammation in these rheumatic diseases, and mechanistic data from mice support a functional role for IL-23-IL-17 pathway activation in the development of enthesitis and in entheseal bone formation. Furthermore, analysis of human tissue samples, as well as data from clinical trials, also supports a role for activation of the IL-23-IL-17 pathway in these diseases. The unique bone phenotype that occurs in PsA and AS is a surprising coexistence of both systemic bone loss and periosteal and entheseal bone formation and is likely to be the result of the actions of IL-23 and/or IL-17 on bone. However, the effects of these cytokines on bone cells are complex, and controversy remains regarding their exact roles in the specific bone microenvironments relevant to PsA and AS. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 17594790
- Volume :
- 14
- Issue :
- 11
- Database :
- Academic Search Index
- Journal :
- Nature Reviews Rheumatology
- Publication Type :
- Academic Journal
- Accession number :
- 132702234
- Full Text :
- https://doi.org/10.1038/s41584-018-0091-8