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Proinflammatory cytokines synergistically enhance the production of chemokine ligand 20 (CCL20) from rheumatoid fibroblast-like synovial cells in vitro and serum CCL20 is reduced in vivo by biologic disease-modifying antirheumatic drugs
Journal of Rheumatology, 10/05/09

Kawashiri SY et al. – Proinflammatory cytokines modulate the production of CCL20 from FLS. Our data suggest that therapeutic efficacy of biologic DMARD may result from the inhibition of CCL20 production in rheumatoid synovium

Methods

In vitro study investigated effect of proinflammatory cytokines and biologic disease-modifying antirheumatic drugs (DMARD) on the production of CCL20 by rheumatoid fibroblast-like synovial cells (FLS)
In vivo role of CCL20 studied by screening for serum CCL20 concentration in patients with RA during therapeutic course of biologic DMARD, i.e., infliximab, etanercept, and tocilizumab

Results

Spontaneous CCL20 production from rheumatoid FLS minimal
Production significantly stimulated by interleukin 1ß (IL-1ß), tumor necrosis factor-? (TNF-?), or IL-17. IL-1ß was most potent for stimulating the production of CCL20
Interferon-? suppressed IL-1ß-induced CCL20 production
IL-6, in combination with soluble IL-6 receptor (sIL-6R), did not modulate CCL20 production, whereas IL-1ß-induced, TNF-?-induced, and IL-17-induced production increased by IL-6
Production levels clearly suppressed by biologic DMARD in vitro
Serum CCL20 significantly higher in RA than in control subjects, was clearly decreased by treatment with infliximab, etanercept, and tocilizumab

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