Tumor necrosis factor priming of peripheral blood neutrophils from rheumatoid arthritis patients

I. C. Kowanko, Antonio Ferrante, G. Clemente, P. P. Youssef, M. Smith

Research output: Contribution to journalArticlepeer-review

13 Citations (Scopus)

Abstract

Recently it was shown that tumor necrosis factor-α (TNF) receptors on neutrophils may be down-regulated after stimulation with proinflammatory mediators. Since in rheumatoid arthritis neutrophils are likely to encounter these mediators in the circulation, we tested the hypothesis that rheumatoid arthritis neutrophil TNF receptors are down-regulated. Peripheral blood neutrophils from patients with rheumatoid arthritis and healthy subjects were compared with respect to their TNF binding activity and ability to be primed by TNF. There were no differences between rheumatoid arthritis and control neutrophils in receptor-mediated TNF binding, superoxide release in response to agonist,and TNF priming of this respiratory burst or in the ability to decade cartilage in vitro and TNF priming for increased cartilage damage. It is evident that rheumatoid arthritis blood neutrophils retain the ability to bind TNF and can be primed by TNF for increased oxygen radical production and augmented cartilage damage. These findings further implicate the role of neutrophils in the pathogenesis of arthritis.

Original languageEnglish
Pages (from-to)216-221
Number of pages6
JournalJournal of Clinical Immunology
Volume16
Issue number4
DOIs
Publication statusPublished - Jul 1996
Externally publishedYes

Keywords

  • Cartilage injury
  • Neutrophil
  • Pathogenesis
  • Priming
  • Receptor
  • Respiratory burst
  • Rheumatoid arthritis
  • Superoxide
  • Tumor necrosis factor

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