Rheumatoid arthritis synovial fibroblasts produce a soluble form of the interleukin-7 receptor in response to pro-inflammatory cytokines.
Bottom Line: We found that exposure of RA FLS to pro-inflammatory cytokines (TNF-α, IL-1β and combinations of TNF-α and IL-1β or TNF-α and IL-17) induces sIL-7R secretion.In DMARD-resistant patients, high sIL-7R serum concentrations are strongly associated with poor response to TNF-blockade.In conclusion, sIL-7R is induced by pro-inflammatory cytokines in RA FLS. sIL-7R could qualify as a new biomarker of response to therapy in RA.
Affiliation: Rheumatology Department, Cliniques Universitaires Saint-Luc, Université catholique de Louvain, Brussels, Belgium.Show MeSH
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Mentions: Synovial overexpression of IL-7R is associated with poor response to TNF blockade in DMARD-resistant RA patients . We therefore wondered whether baseline serum sIL-7R levels would have the same informative value about response to TNF blocking therapy in RA. Strikingly, in patients displaying active disease despite DMARD therapy and subsequently treated with TNF blockade, elevated baseline sIL-7R serum levels strongly predicted poor response to anti-TNF therapy (Fig. 4A, B and C). A total of 55.5% of non-responders to infliximab therapy had an abnormal sIL-7R value at baseline, versus 15.3% of the responders. Conversely, normal baseline sIL-7R serum levels were associated with adequate response to therapy, with a sensitivity of 93% and a specificity of 56%. In case of low sIL-7R serum titres, patients have a 87% probability of being responders (predictive positive value); by contrast, in case of elevated sIL-7R serum levels, patients have a 71% probability of being non-responders (predictive negative value).
Affiliation: Rheumatology Department, Cliniques Universitaires Saint-Luc, Université catholique de Louvain, Brussels, Belgium.