Background Both B cells and TNF have been shown to play an important role in the pathogenesis of rheumatoid arthritis and juvenile idiopathic arthritis (JIA). However, it remains unclear whether these two important players and the therapies that target them are mechanistically linked. In particular, the impact of TNF-α inhibition on the B cell compartment in children with juvenile idiopathic arthritis has not been investigated so far. In adult patients with rheumatoid arthritis, two recent studies demonstrate a decrease in memory B cells as a result of anti-TNF treatment using Etanercept1 or Infliximab2, respectively, in patients with rheumatoid arthritis. However, so far no studies have been performed in patients with JIA in this respect. Changes within the composition of the B cell subpopulations could be a direct effect of Etanercept. Alternatively, it might be caused indirectly through alterations in T cells or BAFF signaling.
Objectives This study was designed to analyze impact of Etanercept therapy on the composition of both the B and T cell compartment and the BAFF system in patients with JIA.
Methods B and T cell subpopulations in the peripheral blood from patients with JIA were investigated by multicolor flow cytometry. Serum BAFF and APRIL levels were determined by ELISA. In addition, standard laboratory parameters including C-reactive protein, whole blood cell count,blood sedimentation rate and immunoglobulin levels were collected.
Results To date, more than 150 patients have been included into the study. Patients are grouped based on current treatment with Etanerpcet, Methotrexate or NSAID. First data demonstrate that treatment with MTX has an effect on the composition of the B cell compartment and leads to slighty decreased total immonoglobulin levels. In contrast, no obvious decrease in memory B cells after TNF inhibition as described in adult patients1,2 with arthritis could be observed in our cohort of JIA patients.
Conclusions Anti-rheumatic therapy has an impact on the B cell compartment in patients with JIA.
Anolik, JH, et al: Cutting edge: anti-tumor necrosis factor therapy in rheumatoid arthritis inhibits memory B lymphocytes via effects on lymphoid germinal centers and follicular dendritic cell networks. J Immunol 2008;180:688.
Souto-Carneiro, MM, et al: Alterations in peripheral blood memory B cells in patients with active rheumatoid arthritis are dependent on the action of tumour necrosis factor. Arthritis Res Ther 2009;11:R84.
Disclosure of Interest None Declared