Thinard Reynald, Farkas Attila E, Halasa Marta, Chevalier Melanie, Brodaczewska Klaudia, Majewska Aleksandra, Zdanowski Robert, Paprocka Maria, Rossowska Joanna, Duc Lam Tri, Greferath Ruth, Krizbai Istvan, Van Leuven Fred, Kieda Claudine, Nicolau Claude
ALSaTECH, Inc., 300 Market Street, Boston, MA 02135, USA.
Institute of Biophysics, Biological Research Centre, Eötvös Lorand Research Network (ELKH), 6726 Szeged, Hungary.
Pharmaceutics. 2022 Jul 6;14(7):1418. doi: 10.3390/pharmaceutics14071418.
The failures of anti-β-amyloid immunotherapies suggested that the very low fraction of injected antibodies reaching the brain parenchyma due to the filtering effect of the BBB may be a reason for the lack of therapeutic effect. However, there is no treatment, as yet, for the amyotrophic lateral sclerosis (ALS) despite substantial evidence existing of the involvement of TDP-43 protein in the evolution of ALS. To circumvent this filtering effect, we have developed a novel approach to facilitate the penetration of antibody fragments (Fabs) into the brain parenchyma. Leveraging the homing properties of endothelial progenitor cells (EPCs), we transfected, ex vivo, such cells with vectors encoding anti-β-amyloid and anti-TDP43 Fabs turning them into an "antibody fragment factory". When injected these cells integrate into the BBB, where they secrete anti-TDP43 Fabs. The results showed the formation of tight junctions between the injected engineered EPCs and the unlabeled resident endothelial cells. When the EPCs were further modified to express the anti-TDP43 Fab, we could observe integration of these cells into the vasculature and the secretion of Fabs. Results confirm that production and secretion of Fabs at the BBB level leads to their migration to the brain parenchyma where they might exert a therapeutic effect.
抗β-淀粉样蛋白免疫疗法的失败表明,由于血脑屏障的过滤作用,注入的抗体仅有极低比例能够到达脑实质,这可能是缺乏治疗效果的原因之一。然而,尽管有大量证据表明TDP-43蛋白参与肌萎缩侧索硬化症(ALS)的发展,但目前尚无针对ALS的治疗方法。为了规避这种过滤作用,我们开发了一种新方法来促进抗体片段(Fabs)进入脑实质。利用内皮祖细胞(EPCs)的归巢特性,我们在体外将编码抗β-淀粉样蛋白和抗TDP43 Fabs的载体转染到这些细胞中,使其成为一个“抗体片段工厂”。当注射这些细胞时,它们会整合到血脑屏障中,并在那里分泌抗TDP43 Fabs。结果显示,注射的工程化EPCs与未标记的驻留内皮细胞之间形成了紧密连接。当EPCs进一步被修饰以表达抗TDP43 Fab时,我们可以观察到这些细胞整合到脉管系统中并分泌Fabs。结果证实,在血脑屏障水平产生和分泌Fabs会导致它们迁移到脑实质,在那里它们可能发挥治疗作用。