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配对抗体与血小板内皮细胞黏附分子-1不同表位结合的协同增强机制

Mechanism of Collaborative Enhancement of Binding of Paired Antibodies to Distinct Epitopes of Platelet Endothelial Cell Adhesion Molecule-1.

作者信息

Kiseleva Raisa, Greineder Colin F, Villa Carlos H, Hood Elizabeth D, Shuvaev Vladimir V, Sun Jing, Chacko Ann-Marie, Abraham Valsamma, DeLisser Horace M, Muzykantov Vladimir R

机构信息

Department of Pharmacology, The Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States of America.

Pulmonary, Allergy & Critical Care Division, The Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States of America.

出版信息

PLoS One. 2017 Jan 13;12(1):e0169537. doi: 10.1371/journal.pone.0169537. eCollection 2017.

Abstract

Monoclonal antibodies (mAbs) directed to extracellular epitopes of human and mouse Platelet Endothelial Cell Adhesion Molecule-1 (CD31 or PECAM-1) stimulate binding of other mAbs to distinct adjacent PECAM-1 epitopes. This effect, dubbed Collaborative Enhancement of Paired Affinity Ligands, or CEPAL, has been shown to enhance delivery of mAb-targeted drugs and nanoparticles to the vascular endothelium. Here we report new insights into the mechanism underlying this effect, which demonstrates equivalent amplitude in the following models: i) cells expressing a full length PECAM-1 and mutant form of PECAM-1 unable to form homodimers; ii) isolated fractions of cellular membranes; and, iii) immobilized recombinant PECAM-1. These results indicate that CEPAL is mediated not by interference in cellular functions or homophilic PECAM-1 interactions, but rather by conformational changes within the cell adhesion molecule induced by ligand binding. This mechanism, mediated by exposure of partially occult epitopes, is likely to occur in molecules other than PECAM-1 and may represent a generalizable phenomenon with valuable practical applications.

摘要

针对人及小鼠血小板内皮细胞黏附分子-1(CD31或PECAM-1)细胞外表位的单克隆抗体(mAb)可刺激其他mAb与不同的相邻PECAM-1表位结合。这种效应被称为配对亲和配体协同增强作用(CEPAL),已被证明可增强mAb靶向药物和纳米颗粒向血管内皮的递送。在此,我们报告了对该效应潜在机制的新见解,该效应在以下模型中表现出相同的幅度:i)表达全长PECAM-1和无法形成同源二聚体的PECAM-1突变形式的细胞;ii)细胞膜的分离组分;以及iii)固定化的重组PECAM-1。这些结果表明,CEPAL不是由细胞功能干扰或PECAM-1同源相互作用介导的,而是由配体结合诱导的细胞黏附分子构象变化介导的。这种由部分隐匿表位暴露介导的机制可能发生在PECAM-1以外的分子中,并且可能代表一种具有宝贵实际应用价值的普遍现象。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8733/5234847/2cec3bbffe8a/pone.0169537.g001.jpg

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