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CD20/TNFR1 dual-targeting antibody enhances lysosome rupture-mediated cell death in B cell lymphoma

Authors
 Jeong Ryeol Kim  ;  Donghyuk Lee  ;  Yerim Kim 1, Joo Young Kim 
Citation
 CANCER IMMUNOLOGY IMMUNOTHERAPY, Vol.72(6) : 1567-1580, 2023-06 
Journal Title
CANCER IMMUNOLOGY IMMUNOTHERAPY
ISSN
 0340-7004 
Issue Date
2023-06
MeSH
Antibodies, Bispecific / pharmacology ; Antigens, CD20 ; Cell Death ; Humans ; Lymphoma, B-Cell* / drug therapy ; Receptors, Tumor Necrosis Factor, Type I / therapeutic use ; Tumor Necrosis Factor-alpha*
Keywords
Antibody binding-induced cell death ; BNHL (B cell non-Hodgkin’s lymphoma) ; Bispecific or fusion proteins ; Obinutuzumab ; TNFR1
Abstract
Obinutuzumab is a therapeutic antibody for B cell non-Hodgkin’s Lymphoma (BNHL), which is a glyco-engineered anti-CD20 antibody with enhanced antibody-dependent cellular cytotoxicity (ADCC) and causes binding-induced direct cell death (DCD) through lysosome membrane permeabilization (LMP). Tumour necrosis factor receptor 1 (TNFR1), a pro-inflammatory death receptor, also evokes cell death, partly through lysosomal rupture. As both obinutuzumab- and TNFR1-induced cell deaths are mediated by LMP and combining TNFR1 and obinutuzumab can amplify LMP-mediated cell death, we made dual-targeting antibody for CD20 and TNFR1 to enhance DCD of obinutuzumab. Obinutuzumab treatment-induced CD20 and TNFR1 colocalisation, and TNFR1-overexpressing cells showed increased obinutuzumab-induced DCD. Two targeting modes, anti-CD20/TNFR1 bispecific antibodies (bsAbs), and obinutuzumab-TNFα fusion proteins (OBI-TNFα
Full Text
https://link.springer.com/article/10.1007/s00262-022-03344-9
DOI
10.1007/s00262-022-03344-9
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Pharmacology (약리학교실) > 1. Journal Papers
Yonsei Authors
Kim, Joo Young(김주영) ORCID logo https://orcid.org/0000-0003-2623-1491
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/198205
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