Tiller Kathryn E, Li Lijuan, Kumar Sandeep, Julian Mark C, Garde Shekhar, Tessier Peter M
From the Center for Biotechnology and Interdisciplinary Studies, Isermann Department of Chemical and Biological Engineering, Rensselaer Polytechnic Institute, Troy, New York 12180 and.
Pharmaceutical Research and Development, Biotherapeutics Pharmaceutical Sciences, Pfizer Inc., Chesterfield, Missouri 63017.
J Biol Chem. 2017 Oct 6;292(40):16638-16652. doi: 10.1074/jbc.M117.783837. Epub 2017 Aug 4.
Antibodies commonly accumulate charged mutations in their complementarity-determining regions (CDRs) during affinity maturation to enhance electrostatic interactions. However, charged mutations can mediate non-specific interactions, and it is unclear to what extent CDRs can accumulate charged residues to increase antibody affinity without compromising specificity. This is especially concerning for positively charged CDR mutations that are linked to antibody polyspecificity. To better understand antibody affinity/specificity trade-offs, we have selected single-chain antibody fragments specific for the negatively charged and hydrophobic Alzheimer's amyloid β peptide using weak and stringent selections for antibody specificity. Antibody variants isolated using weak selections for specificity were enriched in arginine CDR mutations and displayed low specificity. Alanine-scanning mutagenesis revealed that the affinities of these antibodies were strongly dependent on their arginine mutations. Antibody variants isolated using stringent selections for specificity were also enriched in arginine CDR mutations, but these antibodies possessed significant improvements in specificity. Importantly, the affinities of the most specific antibodies were much less dependent on their arginine mutations, suggesting that over-reliance on arginine for affinity leads to reduced specificity. Structural modeling and molecular simulations reveal unique hydrophobic environments near the arginine CDR mutations. The more specific antibodies contained arginine mutations in the most hydrophobic portions of the CDRs, whereas the less specific antibodies contained arginine mutations in more hydrophilic regions. These findings demonstrate that arginine mutations in antibody CDRs display context-dependent impacts on specificity and that affinity/specificity trade-offs are governed by the relative contribution of arginine CDR residues to the overall antibody affinity.
在亲和力成熟过程中,抗体通常会在其互补决定区(CDR)积累带电荷的突变,以增强静电相互作用。然而,带电荷的突变可介导非特异性相互作用,目前尚不清楚CDR在不影响特异性的情况下能在多大程度上积累带电荷的残基以增加抗体亲和力。这对于与抗体多特异性相关的带正电荷的CDR突变尤其令人担忧。为了更好地理解抗体亲和力/特异性的权衡,我们通过对抗体特异性进行弱筛选和严格筛选,选择了对带负电荷且疏水的阿尔茨海默病淀粉样β肽具有特异性的单链抗体片段。使用弱特异性筛选分离出的抗体变体富含精氨酸CDR突变,且特异性较低。丙氨酸扫描诱变显示,这些抗体的亲和力强烈依赖于它们的精氨酸突变。使用严格特异性筛选分离出的抗体变体也富含精氨酸CDR突变,但这些抗体在特异性方面有显著改善。重要的是,最具特异性的抗体的亲和力对其精氨酸突变的依赖性要小得多,这表明过度依赖精氨酸来提高亲和力会导致特异性降低。结构建模和分子模拟揭示了精氨酸CDR突变附近独特的疏水环境。更具特异性的抗体在CDR最疏水的部分含有精氨酸突变,而特异性较低的抗体在更亲水的区域含有精氨酸突变。这些发现表明,抗体CDR中的精氨酸突变对特异性具有上下文依赖性影响,并且亲和力/特异性的权衡受精氨酸CDR残基对整体抗体亲和力的相对贡献的支配。