ArticleArthritis research & therapy2010
Could the expression of CD86 and FcγRIIB on B cells be functionally related and involved in driving rheumatoid arthritis?
Article in Arthritis research & therapy, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed, 7 citations in OpenAlex.
- A Transmembrane Polymorphism of Fcγ Receptor IIb Is Associated with Kidney Deficiency Syndrome in Rheumatoid Arthritis.Evidence-based complementary and alternative medicine : eCAM · 2016Article
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2 authors at 1 institution in 1 country.
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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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