Systemic levels of IL-23 are strongly associated with disease activity in rheumatoid arthritis but not spondyloarthritis

Abstract

Th17-related cytokines are expressed in joints of spondyloarthritis as well as RA patients. IL-23 levels, however, correlate with disease activity parameters in RA only. These results point towards a differential regulation of the Th17 cytokine system in spondyloarthritis compared with RA.

IL-12 Family Cytokines in Inflammation and Bone Erosion of Rheumatoid Arthritis

“…Given that IL-23 shares the same protein subunit of IL-12p40, it can be concluded that IL-23 is the key pathological cytokine in joint inflammation. To support this theory is the discovery of significantly higher levels of IL-23 in both serum and synovial fluid of RA patients (Melis et al, 2010). Results from our unpublished studies with recombinant IL-23 in CIA mice have yielded interesting findings.…”

“…Th17 development is governed by TGF, IL-1 and IL-23 (Paradowska-Gorycka et al, 2010;Santarlasci et al, 2009). Higher concentrations of IL-23 (a member of the IL-12 family cytokines) are detected in the serum and synovial fluid of patients with greater severity of RA (Melis et al, 2010). IL-23 can also be produced by osteoblast cells after stimulation with TNF (unpublished data).…”

IL-23R rs11209026 polymorphism modulates IL-17A expression in patients with rheumatoid arthritis

“…29 The concentrations of the cytokines measured in our study are consistent with those reported in other studies. 30,31 Although IL1b has been shown to correlate with RA disease severity, 32 our data suggest it is largely independent of the other cytokines measured, and tends to be present in large amounts or not at all. This most likely reflects a different inflammatory pathway dominating in these patients.…”

Protective Role of Naturally Occurring Interleukin-17A-Producing γδ T Cells in the Lung at the Early Stage of Systemic Candidiasis in Mice

“…Similar to ␥␦ T cells, Th17 cells express IL-23R, which induces IL-17A production and cell proliferation (2,24). In addition to its protective roles, IL-23 potentially induces autoimmune disorders, such as experimental allergic encephalomyelitis, inflammatory bowel disease (IBD), and rheumatoid arthritis (RA), in which Th17 cells, as well as IL-17A-producing ␥␦ T cells, are involved (8,16,25). In this regard, since responsiveness to IL-23 should be tightly regulated, it is interesting to elucidate the mechanism for maintaining IL-23R expression on IL-17A-producing ␥␦ T cells involved in host defense against systemic C. albicans infection.…”