Kowanko I C, Ferrante A, Clemente G, Youssef P P, Smith M
Department of Immunology, University Department of Paediatrics, Women's and Children's Hospital, North Adelaide, South Australia.
J Clin Immunol. 1996 Jul;16(4):216-21. doi: 10.1007/BF01541227.
Recently it was shown that tumor necrosis factor-alpha (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 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.
最近有研究表明，中性粒细胞上的肿瘤坏死因子-α（TNF）受体在受到促炎介质刺激后可能会下调。由于在类风湿性关节炎中，中性粒细胞很可能在循环中遇到这些介质，因此我们检验了类风湿性关节炎中性粒细胞TNF受体下调这一假说。对类风湿性关节炎患者和健康受试者的外周血中性粒细胞的TNF结合活性以及被TNF激活的能力进行了比较。类风湿性关节炎中性粒细胞与对照中性粒细胞在受体介导的TNF结合、对激动剂的超氧化物释放、TNF引发的呼吸爆发以及体外降解软骨的能力和TNF引发的软骨损伤增加方面均无差异。显然，类风湿性关节炎血液中的中性粒细胞保留了结合TNF的能力，并且可以被TNF激活以增加氧自由基的产生和加剧软骨损伤。这些发现进一步表明了中性粒细胞在关节炎发病机制中的作用。
