TUMOR-NECROSIS-FACTOR PRIMING OF PERIPHERAL-BLOOD NEUTROPHILS FROM RHEUMATOID-ARTHRITIS PATIENTS

Recently it was shown that tumor necrosis factor-alpha (TNF) receptors on neutrophils may be down-regulated after stimulation with proinflam matory mediators. Since in rheumatoid arthritis neutrophils are likely to encounter these mediators in the circulation, we tested the hypoth esis that rheumatoid arthritis neutrophil TNF receptors are down-regul ated. Peripheral blood neutrophils from patients with rheumatoid arthr itis and healthy subjects were compared with respect to their TNF bind ing activity and ability to be primed by TNF. There were no difference s between rheumatoid arthritis and control neutrophils in receptor-med iated TNF binding, superoxide release in response to agonist, and TNF priming of this respiratory burst or in the ability to degrade cartila ge in vitro and TNF priming for increased cartilage damage. It is evid ent that rheumatoid arthritis blood neutrophils retain the ability to bind TNF and can be primed by TNF for increased oxygen radical product ion and augmented cartilage damage. These findings further implicate t he role of neutrophils in the pathogenesis of arthritis.