French L E, Polla L L, Tschopp J, Schifferli J A
Department of Medicine, Hôpital Cantonal Universitaire, Geneva, Switzerland.
J Invest Dermatol. 1992 May;98(5):758-63. doi: 10.1111/1523-1747.ep12499946.
Clusterin and S-protein bind to the membrane attack complex of complement (MAC) rendering it cytolytically inactive. Tissue necrosis as produced by pulsed tunable dye laser therapy (PTDL), and immune complex-related diseases such as lupus erythematosus, are accompanied by local accumulation of MAC. However, the mechanisms responsible for this accumulation might differ, and lead to deposition of MAC in different forms (cytolytically active or inactive). Biopsy specimens of lesional (22) and non-lesional (10) skin from 27 patients with a positive lupus band test (LBT) were studied using monoclonal antibodies against clusterin, S-protein, and MAC by immunofluorescence and immunoperoxidase. Identical studies were performed in normal and angiomatous skin specimens from three normal individuals before and after laser irradiation. MAC was present in 30 of 32 positive LBT skin biopsies. MAC was not only present in lesional (21 of 22) but also in non-lesional skin (nine of 10), although the intensity of staining appeared to be lower in the latter. Clusterin and S-protein co-localized with MAC, respectively, in 20 and 12 specimens, and were not found in the absence of MAC. In addition S-protein deposits were seen only in biopsies positive for clusterin. Deposits of clusterin and S-protein did not correlate with the presence or absence of lesions. After irradiation with PTDL, the immediate complement activation was accompanied by MAC deposits that were granular and clearly located on vascular endothelial cells. Clusterin and S-protein were not present on these cells. In summary, clusterin localizes with MAC along the skin dermal-epidermal junction in patients with a positive LBT, suggesting that it has a similar and possibly more important role than S-protein in regulating immune complex-mediated MAC formation. By contrast, clusterin and S-protein are not involved at the time of MAC formation in cells undergoing necrosis after PTDL therapy.
簇集素和S蛋白与补体膜攻击复合物（MAC）结合，使其失去细胞溶解活性。脉冲可调染料激光治疗（PTDL）产生的组织坏死以及免疫复合物相关疾病（如红斑狼疮）都伴有MAC的局部积聚。然而，导致这种积聚的机制可能不同，并导致MAC以不同形式（细胞溶解活性或无活性）沉积。使用抗簇集素、S蛋白和MAC的单克隆抗体，通过免疫荧光和免疫过氧化物酶对27例狼疮带试验（LBT）阳性患者的2病变皮肤（22例）和非病变皮肤（10例）活检标本进行了研究。在三名正常个体的正常皮肤和血管瘤皮肤标本激光照射前后进行了相同的研究。32例LBT阳性皮肤活检标本中有30例存在MAC。MAC不仅存在于病变皮肤（22例中的21例），也存在于非病变皮肤（10例中的9例），尽管后者的染色强度似乎较低。簇集素和S蛋白分别在20例和12例标本中与MAC共定位，在无MAC的情况下未发现。此外，仅在簇集素阳性的活检标本中可见S蛋白沉积。簇集素和S蛋白的沉积与病变的有无无关。PTDL照射后，即刻补体激活伴有颗粒状且明显位于血管内皮细胞上的MAC沉积。这些细胞上不存在簇集素和S蛋白。总之，在LBT阳性患者中，簇集素与MAC沿皮肤真皮-表皮交界处定位，表明其在调节免疫复合物介导的MAC形成中具有与S蛋白相似且可能更重要的作用。相比之下，在PTDL治疗后发生坏死的细胞中，MAC形成时簇集素和S蛋白不参与。
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