Generation of a blockage monoclonal antibody of LILRB1 against HLA-G

Yunlong Shen; Ruirui Zhang; Xiaohua Jiang; Jinliang Yang

doi:10.1016/j.pep.2023.106363

Generation of a blockage monoclonal antibody of LILRB1 against HLA-G

Protein Expr Purif. 2024 Jan:213:106363. doi: 10.1016/j.pep.2023.106363. Epub 2023 Sep 6.

Authors

Yunlong Shen¹, Ruirui Zhang², Xiaohua Jiang³, Jinliang Yang⁴

Affiliations

¹ State Key Laboratory of Biotherapy and Cancer Center/Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, Chengdu, Sichuan, China. Electronic address: shenyunlongft@163.com.
² State Key Laboratory of Biotherapy and Cancer Center/Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, Chengdu, Sichuan, China. Electronic address: 1741262464@qq.com.
³ State Key Laboratory of Biotherapy and Cancer Center/Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, Chengdu, Sichuan, China. Electronic address: 1258758932@qq.com.
⁴ State Key Laboratory of Biotherapy and Cancer Center/Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, Chengdu, Sichuan, China. Electronic address: jlyang01@163.com.

PMID: 37683901
DOI: 10.1016/j.pep.2023.106363

Abstract

Leukocyte immunoglobulin like receptor B1 (LILRB1) is widely expressed in immune cells as an immunosuppressive receptor. Tumor cells highly express the ligand HLA-G, which inhibits the function of immune cells by binding to LILRB1, to achieve immune escape. LILRB1 is a potential immunotherapeutic target. This study developed a monoclonal antibody named B1M023 (B1M023 mAb) that could bind LILRB1 with high affinity at both protein and cellular levels, while not bind to other leukocyte immunoglobulin like receptors (LILRs). Moreover, B1M023 mAb could block the binding of LILRB1 to HLA-G, promote activation and IFN-γ secretion of T cells. These results indicate that B1M023 mAb has potential applications in concomitant diagnosis and tumor immunotherapy.

Keywords: HLA-G; LILRB1; Monoclonal antibody; T cell activation.