Article Text
Abstract
Background Th17 cells have recently been identified as important in pathogenesis of chronic arthritis including juvenile idiopathic arthritis (JIA). Th17 are highly proinflammatory subset of T cells, characterised by production of interleukin 17 (IL-17/IL-17A). Among members of the IL-17 family designated IL-17A–F, IL-17F is most closely related to IL-17A. IL-17A enhances inflammatory reactions, promotes expansion and recruitment of innate immune cells such as neutrophils. IL-17F induces non-immune cells such as epithelial cells or stromal cells to act proinflammatory. Th17 cells also secrete interleukin-21 (IL-21) and 22 (IL-22).
Objectives The aim of our study was to investigate the profile of Th17 cells producing IL-17A, IL-17F, IL-21, IL-22 in children with juvenile idiopathic arthritis (JIA).
Methods We examined peripheral blood (PB) of 22 patients with JIA (12- female, 9-male) mean age 11±0,7y. Patients were diagnosed according to the ILAR criteria. The type of onset was: oligoarticular – 8, polyarticular – 8, enthesitis related – 6. 8 children submitted to orthopedic surgery acted as a control. The proportion of Th17 cells producing IL-17A, IL-17F, IL-21, IL-22 was performed with multiparameter flow cytometry at two time points, before treatment and in remission.
Results In remission a significant decrease of Th17 compared to the acute phase was found. Analysis IL-17 isoforms of Th17 showed a significant decrease in lymphocytes producing IL-17F (IL-17A-/IL-17F +). There was also a decrease in lymphocytes IL-17A+/IL-17F+, but this result did not reach the level of significance (p = 0.08).
The proportion of cells producing only IL-17A remained unchanged. It is interesting that we found a significant decrease in the proportion of lymphocytes IL-17A+/IL-17F-/IL-21-/IL-22 +.
Conclusions The study shows that in JIA in remission the proportion of Th17 producing IL-17F significantly decreases. The proportion of cells producing only IL-17A remained unchanged, but with the exception of cells producing IL-22 which deceased in remission. In summary, our results would support the hypothesis that activity of Th17 pathway could correlate with proinflammatory activity of non-immune cells.
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Disclosure of Interest None Declared