Sir,
We read with interest the study published by Wang et al. demonstrating the elevated levels of IL-23 and IL-17 in the serum of patients with active Ankylosing Spondylitis (AS) [1].
This illustrates the potential central role of the IL-23/IL-17 axis in AS [2], and is concordant with other findings, such as IL-23 receptor polymorphisms in AS, as well as in Crohn’s disease or in psoriasis [3], sharing the concept of spondyloarthropathy. Elevated IL-17 levels were found in the serum of AS patients [4], and increased numbers of Th 17 cells in the peripheral blood of patients with seronegative spondylarthritides (and not RA) were reported by Jandus [5], as well as increased frequencies of IL-17 positive CD4+ T cells in PBMC from patients with AS [6].
Moreover, for the first time, a higher expression of IL-23 p19 mRNA in PBMC of AS patients as well as enhanced production of IL-17 in the supernatants of PBMC cultured in the presence of recombinant IL-23 was found by Wang et al. [1]. Previous studies did not demonstrate elevated levels of p40 IL-23 in the serum of AS patients, compared with controls, whereas, in some of them, synovial fluid levels were higher than serum levels [7]. This gives the central role to p40 IL-23 in the pathophysiological axis, and a potential theraputic target in AS. Nevertheless, it has been demonstrated that targeting p40 IL-12/23 with a monoclonal antibody (ustekinumab) may be effective in treating psoriatic arthritis [8], psoriasis, and Crohn’s disease.
According to the results of Wang et al. [1], one may speculate that p19 IL-23 blockade may be even more efficacious, and may represent a new therapeutic pathway in AS.
References
Wang X, Lin Z, Wei Q et al (2009) Expression of IL-23 and IL-17 and effect of IL-23 on IL-17 production in ankylosing spondylitis. Rheumatol Int 29:1343–1347
Wendling D (2008) Interleukin 23: a key cytokine in chronic inflammatory disease. Joint Bone Spine 75:517–519
Karaderi T, Harvey D, Farrar C et al (2009) Association between the interleukin 23 receptor and ankylosing spondylitis is confirmed by a new UK case control study and meta-analysis of published series. Rheumatology (Oxford) 48:386–389
Wendling D, Cedoz JP, Racadot E, Dumoulin G (2007) Serum IL-17, BMP-7, and bone turnover markers in patients with ankylosing spondylitis. Joint Bone Spine. 74:304–305
Jandus C, Bioley G, Rivals JP et al (2008) Increased numbers of circulating polyfunctional Th17 memory cells in patients with seronegative spondylarthritides. Arthritis Rheum 58:2307–2317
Shen H, Goodall JC, Hill Gaston JS (2009) Frequency and phenotype of peripheral blood Th17 cells in ankylosing spondylitis and rheumatoid arthritis. Arthritis Rheum 60:1647–1656
Wendling D, Cedoz JP, Racadot E (2009) Serum and synovial fluid levels of p40 IL12/23 in spondyloarthropathy patients. Clin Rheumatol 28:187–190
Gottlieb A, Menter A, Mendelsohn A et al (2009) Ustekinumab, a human interleukin 12/23 monoclonal antibody, for psoriatic arthritis: randomised, double-blind, placebo-controlled, crossover trial. Lancet 373:633–640
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Wendling, D. IL-23 and IL-17 in ankylosing spondylitis. Rheumatol Int 30, 1547 (2010). https://doi.org/10.1007/s00296-009-1226-7
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DOI: https://doi.org/10.1007/s00296-009-1226-7