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首页> 外文期刊>British Journal of Haematology >The induction of immunogenic cell death by type II anti-CD20 monoclonal antibodies has mechanistic differences compared with type I rituximab
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The induction of immunogenic cell death by type II anti-CD20 monoclonal antibodies has mechanistic differences compared with type I rituximab

机译:与I型利妥昔单抗相比,II型抗CD20单克隆抗体诱导的免疫原性细胞死亡具有机理上的差异

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摘要

The anti-CD20 monoclonal antibody (mAb) rituximab has improved outcomes for patients across a range of B-cell malignancies and catalysed the development of a number of other novel anti-CD20 mAb, including the type II anti-CD20 antibody GA101 (Obinutuzumab). GA101 is glycoen-gineered to enhance antibody-dependent cellular cytotoxicity (ADCC) and binds to the CD20 antigen in a fundamentally different way to rituximab to initiate direct Programmed Cell Death (PCD) (Niederfellner et al, 2011) through a novel pathway that is non-apoptotic and dependent on actin rearrangement, lysosomal permeabilisation and reactive oxygen species (ROS) generation via NADPH oxidase and independently of glutathione pathway (Honeychurch et al, 2012).
机译:抗CD20单克隆抗体(mAb)利妥昔单抗改善了一系列B细胞恶性肿瘤的患者预后,并催化了许多其他新型抗CD20 mAb的发展,包括II型抗CD20抗体GA101(Obinutuzumab) 。 GA101经过糖蛋白化处理,增强了抗体依赖性细胞的细胞毒性(ADCC),并以与利妥昔单抗根本不同的方式与CD20抗原结合,从而通过一种新颖的途径引发了直接程序性细胞死亡(PCD)(Niederfellner et al,2011)。非凋亡的并且依赖于肌动蛋白重排,溶酶体通透性和经由NADPH氧化酶生成的活性氧(ROS),并且独立于谷胱甘肽途径(Honeychurch等,2012)。

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