Abstract
In the pathogenesis of rheumatoid arthritis (RA), macrophages (Mφ) play a pivotal role in synovitis, especially at the cartilage–pannus junction. Both Mφ and peripheral blood monocytes (MO) are activated and release proinflammatory cytokines (IL-1β, tumour necrosis factor [TNF] alpha). Neutralization of IL1-β and TNF-α leads to clinical improvement in RA.
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