An in vitro assay for detection of glomerular binding IgG autoantibodies in patients with systemic lupus erythematosus
An in vitro assay for detection of glomerular binding IgG autoantibodies in patients with systemic lupus erythematosus
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DOI：
10.1172/jci118952
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发表时间：
1996-10-01
影响因子：
15.9
通讯作者：
Davidson, A
中科院分区：
文献类型：
--
作者：
Budhai, L;Oh, K;Davidson, A
抗dsDNA抗体在肾小球中的沉积被认为在SLE肾炎的发病机制中起关键作用。然而，血清中抗dsDNA抗体水平与肾脏疾病之间的绝对相关性尚未发现。最近，肾小球结合试验（GBA）已被开发用于检测IgG结合到分离的大鼠肾小球。我们使用GBA研究了四组SLE患者的血清：（A）+抗dsDNA抗体，活动性肾炎;（B）-抗dsDNA抗体，活动性肾炎;（C）+抗dsDNA抗体，无肾炎;和（D）-抗dsDNA抗体，无肾炎。A组和C组患者的血清抗ds-DNA抗体不能根据同种型、电荷或与组蛋白的交叉反应性来区分。然而，肾小球免疫荧光的平均强度显着高于在组A比其他三个患者组和区分血清抗dsDNA抗体的肾炎和那些没有临床上明显的肾炎患者。GBA反应性不受DNA酶处理的血清，但部分抑制预孵育与dsDNA。这些发现与以下假设一致，即一些抗dsDNA抗体与肾小球成分交叉反应，并且这种交叉反应性的存在与肾炎的发展相关，并且可能是肾炎发展的原因。此外，我们已经确定了一组SLE患者的肾脏疾病和典型的肾脏组织病理学和免疫沉积谁没有血清抗dsDNA抗体或抗体，直接结合肾小球GBA。这些患者肾脏免疫沉积的机制仍有待确定。
The deposition of anti-dsDNA antibodies in the glomerulus is believed to play a critical role in the pathogenesis of nephritis in SLE. However, an absolute correlation between serum levels of anti-dsDNA antibodies and renal disease has not been found. Recently a glomerular binding assay (GBA) has been developed to detect IgG binding to isolated rat glomeruli. We have used the GBA to study sera from four groups of SLE patients: (A)+anti-dsDNA antibodies, active nephritis; (B)-anti-dsDNA antibodies, active nephritis; (C)+anti-dsDNA antibodies, no nephritis; and (D)-anti-dsDNA antibodies, no nephritis. The serum antids-DNA antibodies in group A and group C patients could not be distinguished on the basis of isotype, charge, or cross-reactivity with histones. Nevertheless, the mean intensity of glomerular immunofluorescence was significantly higher in group A than in the three other patient groups and distinguished between patients with serum anti-dsDNA antibodies who had nephritis and those without clinically apparent nephritis. GBA reactivity was unaffected by DNase treatment of sera, but was partially inhibited by preincubation with dsDNA. These findings are consistent with the hypothesis that some anti-dsDNA antibodies cross-react with glomerular components and that the presence of this cross-reactivity is associated with, and may be responsible for, the development of nephritis. In addition, we have identified a group of SLE patients with renal disease and typical renal histopathology and immune deposits who do not have serum anti-dsDNA antibodies or antibodies that directly bind to glomeruli in the GBA. The mechanism of renal immune deposition in these patients remains to be determined.