Katayama S, Chia D, Knutson D W, Barnett E V
J Immunol. 1983 Jul;131(1):217-22.
We studied the binding and degradation of stable, soluble heat aggregates of 125I-IgG (A-IgG) by monocytes from 30 patients with systemic lupus erythematosus (SLE) and 30 normals. Relative avidities (KE) for Fc receptor (FcR) binding of A-IgG and maximal binding of A-IgG by monocytes were determined from Scatchard plots of binding data obtained at 4 degrees C. Rates of degradation (Vmax) of A-IgG at 37 degrees C were calculated from Lineweaver-Burke plots of the Michaelis-Menton equation. KE were decreased in SLE monocytes (15.5 X 10(-9) L/M) as compared with normals (20.1 X 10(-9) L/M, p less than 0.005) and Vmax were decreased for SLE (0.89 ng/hr) as compared with normals (1.11 ng/hr, p less than 0.005). The maximal FcR binding by SLE monocytes was not statistically different in SLE patients and normals, but monocytes from SLE patients with active disease showed a lower maximal binding capacity for A-IgG (4.9 ng/10(5) cells) than normals (5.4 ng/10(5) cells, p less than 0.05). KE and Vmax in SLE were also lower for patients with active disease than for normal subjects. KE in patients whose anti-ssDNA binding was greater than 20% were lower than for those with DNA binding of less than 20% (p less than 0.005). These data suggest that patients with active SLE have diminished numbers of available FcR on their circulating monocytes, possibly due to interiorization of FcR during endocytosis of endogenous circulating immune complexes.
我们研究了30例系统性红斑狼疮(SLE)患者和30名正常人的单核细胞对125I标记的稳定、可溶性热聚集IgG(A-IgG)的结合及降解情况。通过4℃下获得的结合数据的Scatchard图确定A-IgG与Fc受体(FcR)结合的相对亲和力(KE)以及单核细胞对A-IgG的最大结合量。根据米氏方程的Lineweaver-Burke图计算37℃时A-IgG的降解速率(Vmax)。与正常人(20.1×10⁻⁹L/M,p<0.005)相比,SLE患者单核细胞的KE降低(15.5×10⁻⁹L/M);与正常人(1.11 ng/hr,p<0.005)相比,SLE患者的Vmax降低(0.89 ng/hr)。SLE患者单核细胞的最大FcR结合量与正常人相比无统计学差异,但活动性疾病的SLE患者单核细胞对A-IgG的最大结合能力(4.9 ng/10⁵细胞)低于正常人(5.4 ng/10⁵细胞,p<0.05)。活动性疾病的SLE患者的KE和Vmax也低于正常受试者。抗单链DNA结合大于20%的患者的KE低于DNA结合小于20%的患者(p<0.005)。这些数据表明,活动性SLE患者循环单核细胞上可用FcR数量减少,可能是由于内源性循环免疫复合物内吞过程中FcR内化所致。