Skip to content


  • Poster presentation
  • Open Access

Characterization of B cells in synovial fluid and tissue from patients with JIA

  • 1,
  • 2,
  • 1,
  • 3,
  • 1,
  • 2 and
  • 1
Pediatric Rheumatology20086 (Suppl 1) :P21

  • Published:


  • Synovial Fluid
  • Synovial Tissue
  • Inflame Joint
  • CCR9 Expression
  • Switch Memory


The nature of B cell subsets infiltrating the synovial membrane from JIA patients is poorly defined. To this aim we performed an immunophenotypic and functional characterization of B cells in JIA patients.


MNC from synovial fluid (SF) and paired peripheral blood (PB) from 25 JIA patients and 20 age-matched controls were analyzed with multi-colour flow cytometry.


SF B cells were found to be significantly enriched in CD27+ switch memory (sm) 1 cells and in the recently identified isotype class switch memory (CD19+CD27-IgG+IgA+) B cells (sm2) compared to paired and healthy PB (P < 0.0001). CCR5, CCR8, and CCR9 expression was significantly higher on SF sm1 and sm2 B cells than on correspondent paired PB B cells (P < 0.001). Naïve (IgD+, CD27-) B cells were significantly reduced in SF compared to paired and control PB (P < 0.0001). Similarly, transitional B cells (CD19+CD24highCD38highIgMhighIgDhigh) were significantly less numerous in SF than in paired PB from JIA patients (P < 0.0001).

Plasma blasts were significantly enriched in SF than in paired PB (P = 0.005). ELISPOT experiments showed significantly higher proportions of CD19+ IgG secreting cells in SF vs paired JIA PB (P = 0.028). Histological analysis of synovial tissue sections demonstrated the presence of lymphoid aggregates containing clusters of CD20+ cells surrounded by CD138+plasmablasts/plasmacells producing predominantly IgG.


These findings support a model whereby memory B cells are selectively attracted through chemokine gradients to the inflamed joints of JIA patients and differentiate locally into plasmablasts/plasmacells in the absence of ectopic follicular structures.

Authors’ Affiliations

UO Pediatria II, G. Gaslini and Laboratory of Immunology of Rheumatic diseases, University of Genoa, Genoa, Italy
Laboratory of Oncology, G. Gaslini Institute, Genoa, Italy
UO Anatomia Patologica, G. Gaslini Institute, Genoa, Italy


© Ferlito et al; licensee BioMed Central Ltd. 2008

This article is published under license to BioMed Central Ltd.