Corsini A, Roma P, Sommariva D, Fumagalli R, Catapano A L
J Clin Invest. 1986 Oct;78(4):940-6. doi: 10.1172/JCI112684.
We studied a 32-yr-old man with a benign paraproteinemia (IgA) affected by severe nonfamilial hypercholesterolemia. In vitro experiments demonstrated that lipoprotein-deficient serum (LPDS) from the patient inhibited the binding of low density lipoprotein (LDL) to human skin fibroblasts cultured in vitro (up to 70%) whereas LPDS from controls had no effect. Removal of IgA from the patient's serum by immunoprecipitation with mono-specific antisera abolished the inhibition of LDL binding. IgA isolated from the serum of the patient by affinity chromatography inhibited, in a dose-dependent manner, the binding of LDL to human skin fibroblasts in vitro, thus showing an IgA-mediated effect. Ligand-blotting experiments demonstrated that the paraprotein directly interacts with the LDL receptor, thus inhibiting the binding of the lipoprotein. Treatment of the receptor protein with reducing agents blocked the interaction of the antibody with the LDL receptor. From these data we speculate that this autoantibody may be responsible for the severe nonfamilial hypercholesterolemia of the patient.
我们研究了一名32岁患有良性副蛋白血症(IgA)且患有严重非家族性高胆固醇血症的男性。体外实验表明,该患者的脂蛋白缺乏血清(LPDS)可抑制低密度脂蛋白(LDL)与体外培养的人皮肤成纤维细胞的结合(高达70%),而对照组的LPDS则无此作用。用单特异性抗血清进行免疫沉淀去除患者血清中的IgA后,LDL结合抑制作用消失。通过亲和层析从患者血清中分离出的IgA以剂量依赖方式抑制LDL与体外培养的人皮肤成纤维细胞的结合,从而显示出IgA介导的效应。配体印迹实验表明,副蛋白直接与LDL受体相互作用,从而抑制脂蛋白的结合。用还原剂处理受体蛋白可阻断抗体与LDL受体的相互作用。根据这些数据,我们推测这种自身抗体可能是该患者严重非家族性高胆固醇血症的病因。