Could the expression of CD86 and FcγRIIB on B cells be functionally related and involved in driving rheumatoid arthritis?
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.
Mauri
Claudia
C
Jury
Elizabeth C
EC
D001172:Arthritis, Rheumatoid / Q000276:immunology*; D051940:B7-2 Antigen / Q000276:immunology*; D015415:Biomarkers; D006801:Humans; D007156:Immunologic Memory / Q000276:immunology*; D017452:Receptors, IgG / Q000276:immunology*
D051940:B7-2 Antigen; D015415:Biomarkers; C497964:CD86 protein, human; C499173:FCGR2B protein, human; D017452:Receptors, IgG