Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/14695
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Type: Journal article
Title: Tumor necrosis factor priming of peripheral blood neutrophils from rheumatoid arthritis patients
Author: Kowanko, I.
Ferrante, A.
Clemente, G.
Youssef, P.
Smith, M.
Citation: Journal of Clinical Immunology, 1996; 16(4):216-221
Publisher: PLENUM PUBL CORP
Issue Date: 1996
ISSN: 0271-9142
1573-2592
Statement of
Responsibility: 
I. C. Kowanko, A. Ferrante, G. Clemente, P. P. Youssef and M. Smith
Abstract: Recently it was shown that tumor necrosis factor-agr (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 degrade cartilagein 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.
Keywords: Tumor necrosis factor
receptor
neutrophil
priming
rheumatoid arthritis
superoxide
respiratory burst
cartilage injury
pathogenesis
Rights: © 1996 Plenum Publishing Corporation
DOI: 10.1007/BF01541227
Appears in Collections:Aurora harvest 7
Nursing publications

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