首页> 美国卫生研究院文献>Annals of the Rheumatic Diseases >Defective responsiveness to ascorbic acid of neutrophil random and chemotactic migration in Feltys syndrome and systemic lupus erythematosus.
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Defective responsiveness to ascorbic acid of neutrophil random and chemotactic migration in Feltys syndrome and systemic lupus erythematosus.

机译:Feltys综合征和系统性红斑狼疮对嗜中性粒细胞随机和趋化迁移对抗坏血酸的不良反应。

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摘要

Polymorphonuclear (PMN) leucocytes from 4 patients with untreated systemic lupus erythematosus (SLE) showed defective random migration (P less than 0-05) and depressed chemotactic responses to C5a and kallikrein (P less than 0-01) compared to PMN leucocytes from normal subjects, or patients with rheumatoid arthritis (4) or Felty's syndrome (4) when examined at a standardized cell concentration with a micropore filter radioassay but not with a conventional Boyden technique. Normal in vitro enhancement of PMN leucocyte random and chemotactic migration by sodium ascorbate was absent in SLE and Felty's syndrome, but sodium ascorbate gave normal stimulation of hexose monophosphate shunt activity in the PMN leucocytes precluding a defect in ascorbate transport.
机译:与正常PMN白细胞相比,来自4例未经治疗的系统性红斑狼疮(SLE)患者的多形核(PMN)白细胞显示出不良的随机迁移(P小于0-05)和对C5a和激肽释放酶的趋化反应抑制(P小于0-01)。受试者或类风湿性关节炎(4)或费氏综合症(4)的患者,通过标准的细胞浓度通过微孔滤光片放射分析法进行检查,但不使用常规的Boyden技术进行检查。 SLE和Felty's综合征缺乏正常的体外抗坏血酸钠增强PMN白细胞随机性和趋化性迁移的能力,但抗坏血酸钠可正常刺激PMN白细胞中的己糖一磷酸分流活性,从而排除了抗坏血酸转运的缺陷。

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