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Publication Detail
Could the expression of CD86 and FcγRIIB on B cells be functionally related and involved in driving rheumatoid arthritis?
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Editorial
  • Authors:
    Mauri C, Jury EC
  • Publication date:
    2010
  • Pagination:
    133, ?
  • Journal:
    Arthritis Res Ther
  • Volume:
    12
  • Issue:
    4
  • Status:
    Published
  • Country:
    England
  • PII:
    ar3092
  • Language:
    eng
  • Keywords:
    Arthritis, Rheumatoid, B7-2 Antigen, Biomarkers, Humans, Immunologic Memory, Receptors, IgG
Abstract
Aberrant immune responses play a pivotal role in the processes that cause inflammation and joint damage in patients with rheumatoid arthritis (RA). Polyclonal B cell activation and the production of autoantibodies are immunological hallmarks of the disease. However, controversy surrounds the pathogenicity of autoantibodies, mainly because not all patients are seropositive (10% of RA patients are seronegative), suggesting that they could be markers rather than makers of disease. Catalán and collaborators report that patients with RA display reduced expression of FcγRIIB on memory B cells and plasma cells, which inversely correlates with autoantibody levels. Considering that FcγRIIB stimulation down-regulates antibody production, this work strengthens the link between autoantibodies and pathogenicity.
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