Journal
ANNALS OF MEDICINE
Volume 43, Issue 7, Pages 503-511Publisher
TAYLOR & FRANCIS LTD
DOI: 10.3109/07853890.2011.577093
Keywords
Cytokines; interleukin-23; rheumatoid arthritis; spondyloarthritis; T cells
Categories
Funding
- Arthritis-Fondation Courtin (France)
- Agence nationale de la recherche (ANR, France)
- Inserm (France)
- Societe francaise de rhumatologie
- University Paris 13
- DGA
- Andar
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Interleukin-23 (IL-23) is a pro-inflammatory cytokine composed of two subunits, p19 and p40. The p40 subunit is shared with IL-12. IL-23 and IL-12 have different receptors and different effects. Whereas IL-12 induces development of Th1 cells, which produce interferon-gamma, IL-23 is involved in differentiation of Th17 cells in a pro-inflammatory context and especially in the presence of TGF-beta and IL-6. Activated Th17 cells produce IL-17A, IL-17F, IL-6, IL-22, TNF-alpha, and GM-CSF. Inflammatory macrophages express IL-23R and are activated by IL-23 to produce IL-1, TNF-alpha, and IL-23 itself. These effects identify IL-23 as a central cytokine in autoimmunity and a highly promising treatment target for inflammatory diseases. IL-23 is found in the skin of patients with psoriasis, in the bowel wall of patients with chronic inflammatory bowel disease, and in synovial membrane of patients with rheumatoid arthritis. IL-23 is involved in osteoclastogenesis, independently from IL-17, via induction of RANKL expression. Debate continues to surround the role for IL-23 in the pathophysiology of inflammatory joint diseases (rheumatoid arthritis and spondyloarthritis). Ustekinumab, which inhibits IL-12 and IL-23 by blocking p40, has been found effective in cutaneous psoriasis and psoriatic arthritis, as well as in Crohn's disease. Treatments that specifically target IL-23 (antibodies to p19) are being developed.
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