Goetzl E J
Ann Rheum Dis. 1976 Dec;35(6):510-5. doi: 10.1136/ard.35.6.510.
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.
与正常受试者、类风湿性关节炎患者(4例)或费尔蒂综合征患者(4例)的多形核(PMN)白细胞相比,4例未经治疗的系统性红斑狼疮(SLE)患者的PMN白细胞在标准化细胞浓度下通过微孔滤膜放射测定法检测时,随机迁移存在缺陷(P<0.05),对C5a和激肽释放酶的趋化反应降低(P<0.01),但采用传统的博伊登技术检测时无此现象。在SLE和费尔蒂综合征中,抗坏血酸钠对PMN白细胞随机和趋化迁移的正常体外增强作用缺失,但抗坏血酸钠能正常刺激PMN白细胞中的磷酸己糖旁路活性,排除了抗坏血酸转运缺陷。