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基导向的PD-1/PD-L1结合的干扰增加了B淋巴细胞在传染性病病毒感染后的功能

Qiuyu Zhang¹, Guopeng Sun², Feng Yue²

¹College of Veterinary Medicine, Henan Agricultural University, Zhengzhou 450046, China; College of Veterinary Medicine, Shanxi Agricultural University, Jinzhong 030801, China.

Poultry science

|October 20, 2024

概括

一种新型的基,CgK-16,有效地破坏了编程细胞死亡蛋白1 (PD-1) /PD-1干1 (PD-L1) 的结合. 这种可以恢复B淋巴细胞的功能,并有可能预防由传染性病病毒 (IBDV) 引起的免疫抑制.

科学领域:

免疫学免疫学免疫学
病毒学病毒学
类治疗药物类治疗药物

背景情况:

编程细胞死亡蛋白1 (PD-1) /PD-1连接物1 (PD-L1) 结合驱动慢性病毒感染的免疫逃避,如传染性突发性疾病病毒 (IBDV),导致B淋巴细胞耗尽和亡.
中的IBDV感染会增加PD-1和PD-L1在外周血液单核细胞中的表达.
目前针对PD-1/PD-L1的单克隆抗体疗法因成本和不良事件而受到限制,需要采用替代策略.

研究的目的:

设计可以抑制PD-1/PD-L1结合并恢复B淋巴细胞功能的.
评估新CGK-16在破坏PD-1/PD-L1相互作用和减轻IBDV诱导的免疫抑制中的有效性.

主要方法:

针对PD-1结合部位的的设计和合成.
在体外评估对PD-1的亲和力和抑制PD-1/PD-L1相互作用.
评估CgK-16对IBDV感染细胞中的B淋巴细胞增殖,亡,NF-κB激活,PI3K/AKT通路和免疫球蛋白M (IgM) 生产的影响.

主要成果:

基KK-16对PD-1具有很高的亲和力 (K_D:3.37nM),并且在体外有效抑制了PD-1/PD-L1的相互作用.
gCK-16显著增强了B淋巴细胞的增殖,并取消了IBDV诱导的PD-1/PD-L1,NF-κB激活和B淋巴细胞亡的上调.
gCK-16治疗恢复了PI3K/AKT通路的激活,并在IBDV感染的B淋巴细胞中增加了IgM的产生.

结论:

基CGK-16在恢复B淋巴细胞功能以抵抗IBDV感染方面显示出显著的潜力.
gCK-16是预防IBDV引起的禽类免疫抑制的有希望的治疗候选者.
这些发现支持CGK-16作为抗击IBDV诱导免疫抑制的疫苗辅助剂的发展.

关键词:

B 淋巴细胞的功能在PD-1/PD-L1中.免疫抑制是一种免疫抑制.传染性牛皮病病毒感染的病毒.化物CGK-16 是一种

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