Abstract

IntroductionDisturbances in peripheral blood memory B cell subpopulations have been observed in various autoimmune diseases, but have not been fully delineated in rheumatoid arthritis (RA). Additionally, the possible role of tumour necrosis factor (TNF) in regulating changes in specific peripheral blood memory B cell subsets in RA is still unclear.MethodsThe frequency and distribution of B cell subsets in the peripheral blood and synovial membrane of active RA patients with long-standing disease have been analysed. Additionally, the possible role of TNF in causing disturbances in memory B cell subsets in RA patients was assessed in a clinical trial with the specific TNF-neutralising antibody, infliximab.ResultsRA patients, independent of disease duration, have a significantly lower frequency of peripheral blood pre-switch IgD+CD27+ memory B cells than healthy individuals, whereas post-switch IgD-CD27+ accumulate with increased disease duration. Notably, both pre-switch IgD+CD27+ and post-switch IgD-CD27+ memory B cells accumulate in the synovial membrane of RA patients. Finally, anti-TNF therapy increased the frequency of pre-switch IgD+CD27 memory B cells in the peripheral blood.ConclusionsThe data suggest that decreases in peripheral blood IgD+CD27+ pre-switch memory B cells in RA reflect their accumulation in the synovial tissue. Moreover, the significant increase in the peripheral blood pre-switch memory B cells in patients who underwent specific TNF-blockade with infliximab indicates that trafficking of memory B cells into inflamed tissue in RA patients is regulated by TNF and can be corrected by neutralising TNF.

Highlights

  • Introduction Disturbances in peripheral blood memoryB cell subpopulations have been observed in various autoimmune diseases, but have not been fully delineated in rheumatoid arthritis (RA)

  • The data suggest that decreases in peripheral blood IgD+CD27+ pre-switch memory B cells in RA reflect their accumulation in the synovial tissue

  • The significant increase in the peripheral blood pre-switch memory B cells in patients who underwent specific tumour necrosis factor (TNF)-blockade with infliximab indicates that trafficking of memory B cells into inflamed tissue in RA patients is regulated by TNF and can be corrected by neutralising TNF

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Summary

Introduction

Introduction Disturbances in peripheral blood memoryB cell subpopulations have been observed in various autoimmune diseases, but have not been fully delineated in rheumatoid arthritis (RA). APC: allophycocyanin; BSA: bovine serum albumin; CRP: C-reactive protein; DMARD: disease-modifying anti-rheumatic drugs; DMEM: Dulbecco's Modified Eagle's Medium; ELISA: enzyme-linked immunosorbent assay; ESR: erythrocyte sedimentation rate; FCS: fetal calf serum; FDC: follicular dendritic cell; FITC: fluorescein isothiocyanate; ICAM: intercellular adhesion molecule; IgVH: immunoglobulin heavy chain variable region; IL: interleukin; LT: lymphotoxin; MAb: monoclonal antibodies; MTX: methotrexate; PBMC: peripheral blood mononuclear cells; PBS: phosphate-buffered saline; PCR: polymerase chain reaction; PE: phycoerythrin; PerCpCy5.5: peridinin-chlorophyll-protein Cy5.5; RA: rheumatoid arthritis; SLE: systemic lupus erythematosus; SS: Sjögren's syndrome; TNF: tumour necrosis factor; VCAM: vascular cell adhesion molecule; VEGF: vascular endothelial growth factor. In RA the data on possible disturbances of peripheral blood B cell distributions have not been delineated as well Part of this could relate to differences in disease duration and therapy of the cohorts studied [19,20,21]

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