Kolb H, Friedrich E, Süss R
Hoppe Seylers Z Physiol Chem. 1981 Dec;362(12):1609-14. doi: 10.1515/bchm2.1981.362.2.1609.
Mammalian erythrocytes loose their normal circulatory pattern following desialylation by sialidase and are trapped in the liver. The mechanism responsible for this phenomenon has been studied by a new scintigraphic method. We report here that the retention of asialo-erythrocytes in the liver is due to the interaction between a lectin-like receptor on Kupffer cells and terminal D-galactosyl residues exposed on erythrocytes after sialidase treatment. The major findings supporting the conclusion are: First, kinetics of asialo-erythrocyte accumulation in the liver are identical in conventional and germfree animals, demonstrating that the presence of serum antibody is not essential. Second, trapping of asialo-erythrocytes can be substantially inhibited by intravenous injection of N-acetyl-D-galactosamine or galactosylated bovine serum albumin, other saccharides or glycoproteins are less or not at all effective. This specificity pattern is characteristic for the D-galactose-specific lectin on Kupffer cells. It therefore appears that the retention of sialidase-treated erythrocytes in the liver is lectin- and not antibody mediated.
哺乳动物红细胞经唾液酸酶去唾液酸化后会失去其正常循环模式，并被困在肝脏中。一种新的闪烁扫描法已对导致这种现象的机制进行了研究。我们在此报告，去唾液酸红细胞在肝脏中的滞留是由于库普弗细胞上的一种凝集素样受体与唾液酸酶处理后红细胞表面暴露的末端D-半乳糖基残基之间的相互作用。支持该结论的主要发现如下：第一，常规动物和无菌动物肝脏中去唾液酸红细胞的积累动力学相同，这表明血清抗体的存在并非必需。第二，静脉注射N-乙酰-D-半乳糖胺或半乳糖基化牛血清白蛋白可显著抑制去唾液酸红细胞的捕获，其他糖类或糖蛋白的抑制作用较小或根本没有作用。这种特异性模式是库普弗细胞上D-半乳糖特异性凝集素的特征。因此，经唾液酸酶处理的红细胞在肝脏中的滞留似乎是由凝集素介导而非抗体介导的。
