Daha M R, Westedt M L, Bos B, Krol M C, van Es L A, Cats A
Dept. of Nephrology and Rheumatology, University Hospital, Leiden, The Netherlands.
J Rheumatol. 1987 Aug;14(4):680-5.
We investigated the capacity of monocytes to degrade soluble aggregates of IgG in vitro in the absence (Fc receptor [FcR] mediated) and presence of complement (FcR and C3 receptor mediated). Adherent monocytes from 33 patients with active rheumatoid arthritis (RA) and rheumatoid vasculitis, 32 patients with inactive RA alone, and 20 healthy controls were incubated with 125I-aggregated IgG (125I-AIgG) of restricted size with or without fresh serum. Normal monocytes degraded 9.8% of 125I-AIgG via FcR alone and the presence of complement enhanced degradation to 2.7%. Degradation of 125I-AIgG via FcR from patients without active RA suggested a depressed function of FcR. The maximal amount of 125I-AIgG which was bound by monocytes from patients with inactive and active RA, however, was increased compared to normals, suggesting a defect in intracellular processing in patients with RA. The degradation of 125I-AIgG in the presence of complement was also significantly depressed for both groups of patients. The monocytes from the patients also had decreased numbers of C3b receptors (CR1). Since CR1 are involved in the enhanced uptake of immune complexes bearing complement, the depressed capacity of monocytes from patients with RA to degrade 125I-AIgG in vitro may be caused both by a diminished uptake as well as a diminished capacity to degrade soluble AIgG.
我们研究了单核细胞在体外降解IgG可溶性聚集体的能力，分别在无补体（Fc受体[FcR]介导）和有补体（FcR和C3受体介导）的情况下进行。将来自33例活动性类风湿关节炎（RA）和类风湿血管炎患者、32例仅患有非活动性RA的患者以及20名健康对照的贴壁单核细胞与大小受限的125I-聚集IgG（125I-AIgG）一起孵育，添加或不添加新鲜血清。正常单核细胞仅通过FcR可降解9.8%的125I-AIgG，补体的存在可将降解率提高至27%。来自无活动性RA患者的单核细胞通过FcR对125I-AIgG的降解表明FcR功能降低。然而，与正常人相比，来自非活动性和活动性RA患者的单核细胞结合的125I-AIgG的最大量增加，提示RA患者存在细胞内处理缺陷。两组患者在有补体存在的情况下对125I-AIgG的降解也显著降低。患者的单核细胞C3b受体（CR1）数量也减少。由于CR1参与增强对带有补体的免疫复合物的摄取，RA患者单核细胞在体外降解125I-AIgG的能力降低可能是由于摄取减少以及降解可溶性AIgG的能力降低所致。
