Abstract
Extra-articular or systemic features occur commonly in seropositive erosive rheumatoid arthritis (RA). Clinical, pathological and immunogenetic evidence suggests that nodule formation, vasculitis and Felty's syndrome can be considered as manifestations of the same fundamental disease process as rheumatoid synovitis. However, while synovitis seems likely to be driven by macrophage activation induced by Th1 cells, systemic involvement in RA is characterised by B cell overactivity, immune complex formation and complement consumption, suggesting that Th2 cells are involved in the pathogenesis of extra-articular rheumatoid disease.
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