Bewarder Moritz, Kiefer Maximilian, Will Helene, Olesch Kathrin, Moelle Clara, Stilgenbauer Stephan, Christofyllakis Konstantinos, Kaddu-Mulindwa Dominic, Bittenbring Joerg Thomas, Fadle Natalie, Regitz Evi, Kaschek Lea, Hoth Markus, Neumann Frank, Preuss Klaus-Dieter, Pfreundschuh Michael, Thurner Lorenz
José Carreras Center for Immuno- and Gene Therapy, Saarland University Medical Center, Homburg, Germany.
Internal Medicine I, Saarland University Medical Center, Homburg, Germany.
Hemasphere. 2021 Jul 13;5(8):e620. doi: 10.1097/HS9.0000000000000620. eCollection 2021 Aug.
Mantle cell lymphoma (MCL) accounts for 5%-10% of all lymphomas. The disease's genetic hallmark is the t(11; 14)(q13; q32) translocation. In younger patients, the first-line treatment is chemoimmunotherapy followed by autologous stem cell transplantation. Upon disease progression, novel and targeted agents such as the BTK inhibitor ibrutinib, the BCL-2 inhibitor venetoclax, or the combination of both are increasingly used, but even after allogeneic stem cell transplantation or CAR T-cell therapy, MCL remains incurable for most patients. Chronic antigenic stimulation of the B-cell receptor (BCR) is thought to be essential for the pathogenesis of many B-cell lymphomas. LRPAP1 has been identified as the autoantigenic BCR target in about 1/3 of all MCLs. Thus, LRPAP1 could be used to target MCL cells, however, there is currently no optimal therapeutic format to integrate LRPAP1. We have therefore integrated LRPAP1 into a concept termed BAR, for B-cell receptor antigens for reverse targeting. A bispecific BAR body was synthesized consisting of the lymphoma-BCR binding epitope of LRPAP1 and a single chain fragment targeting CD3 or CD16 to recruit/engage T or NK cells. In addition, a BAR body consisting of an IgG1 antibody and the lymphoma-BCR binding epitope of LRPAP1 replacing the variable regions was synthesized. Both BAR bodies mediated highly specific cytotoxic effects against MCL cells in a dose-dependent manner at 1-20 µg/mL. In conclusion, LRPAP1 can substitute variable antibody regions in different formats to function in a new therapeutic approach to treat MCL.
套细胞淋巴瘤(MCL)占所有淋巴瘤的5%-10%。该疾病的遗传特征是t(11; 14)(q13; q32)易位。在年轻患者中,一线治疗是化疗免疫疗法,随后进行自体干细胞移植。疾病进展时,越来越多地使用新型靶向药物,如BTK抑制剂伊布替尼、BCL-2抑制剂维奈克拉或两者联合使用,但即使经过异基因干细胞移植或CAR T细胞疗法,大多数患者的MCL仍然无法治愈。B细胞受体(BCR)的慢性抗原刺激被认为是许多B细胞淋巴瘤发病机制的关键。在约1/3的所有MCL中,LRPAP1已被确定为自身抗原性BCR靶点。因此,LRPAP1可用于靶向MCL细胞,然而,目前尚无整合LRPAP1的最佳治疗形式。因此,我们将LRPAP1整合到一个名为BAR的概念中,即用于反向靶向的B细胞受体抗原。合成了一种双特异性BAR体,其由LRPAP1的淋巴瘤-BCR结合表位和靶向CD3或CD16的单链片段组成,以募集/激活T细胞或NK细胞。此外,还合成了一种由IgG1抗体和LRPAP1的淋巴瘤-BCR结合表位取代可变区组成的BAR体。两种BAR体均以1-20 µg/mL的剂量依赖性方式介导对MCL细胞的高度特异性细胞毒性作用。总之,LRPAP1可以替代不同形式的可变抗体区,在治疗MCL的新治疗方法中发挥作用。