Carlson Coby B, Mowery Patricia, Owen Robert M, Dykhuizen Emily C, Kiessling Laura L
Department of Chemistry, University of Wisconsin-Madison, Madison, Wisconsin 53706, USA.
ACS Chem Biol. 2007 Feb 20;2(2):119-27. doi: 10.1021/cb6003788. Epub 2007 Feb 26.
This report highlights the advantages of low-affinity, multivalent interactions to recognize one cell type over another. Our goal was to devise a strategy to mediate selective killing of tumor cells, which are often distinguished from normal cells by their higher levels of particular cell surface receptors. To test whether multivalent interactions could lead to highly specific cell targeting, we used a chemically synthesized small-molecule ligand composed of two distinct motifs: (1) an Arg-Gly-Asp (RGD) peptidomimetic that binds tightly (Kd approximately 10(-9)M) to alphavbeta3 integrins and (2) the galactosyl-alpha(1-3)galactose (alpha-Gal epitope), which is recognized by human anti-alpha-galactosyl antibodies (anti-Gal). Importantly, anti-Gal binding requires a multivalent presentation of carbohydrate residues; anti-Gal antibodies interact weakly with the monovalent oligosaccharide (Kd approximately 10(-5)M) but bind tightly (Kd approximately 10(-11) M) to multivalent displays of alpha-Gal epitopes. Such a display is generated when the bifunctional conjugate decorates a cell possessing a high level of alphavbeta3 integrin; the resulting cell surface, which presents many alpha-Gal epitopes, can recruit anti-Gal, thereby triggering complement-mediated lysis. Only those cells with high levels of the integrin receptor are killed. In contrast, doxorubicin tethered to the RGD-based ligand affords indiscriminate cell death. These results highlight the advantages of exploiting the type of the multivalent recognition processes used by physiological systems to discriminate between cells. The selectivity of this strategy is superior to traditional, abiotic, high-affinity targeting methods. Our results have implications for the treatment of cancer and other diseases characterized by the presence of deleterious cells.
本报告强调了低亲和力多价相互作用在识别一种细胞类型与另一种细胞类型方面的优势。我们的目标是设计一种策略来介导肿瘤细胞的选择性杀伤,肿瘤细胞通常因其特定细胞表面受体水平较高而与正常细胞区分开来。为了测试多价相互作用是否能导致高度特异性的细胞靶向,我们使用了一种化学合成的小分子配体,它由两个不同的基序组成:(1)一种与αvβ3整合素紧密结合(解离常数Kd约为10^(-9)M)的精氨酸-甘氨酸-天冬氨酸(RGD)拟肽;(2)半乳糖基-α(1-3)半乳糖(α-Gal表位),它可被人抗α-半乳糖基抗体(抗-Gal)识别。重要的是,抗-Gal结合需要碳水化合物残基的多价呈现;抗-Gal抗体与单价寡糖的相互作用较弱(Kd约为10^(-5)M),但与α-Gal表位的多价展示紧密结合(Kd约为10^(-11)M)。当双功能缀合物修饰具有高水平αvβ3整合素的细胞时,就会产生这样的展示;由此产生的呈现许多α-Gal表位的细胞表面可以募集抗-Gal,从而触发补体介导的细胞裂解。只有那些整合素受体水平高的细胞才会被杀死。相比之下,与基于RGD的配体相连的阿霉素会导致非选择性的细胞死亡。这些结果突出了利用生理系统用于区分细胞的多价识别过程类型的优势。这种策略的选择性优于传统的非生物高亲和力靶向方法。我们的结果对癌症和其他以有害细胞存在为特征的疾病的治疗具有启示意义。