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生物工程人工细胞外囊呈现PD-L1和Gal-9 改善新发型1型糖尿病

Zhaoxin Yang¹, Zhirang Zhang¹, Liyan Li¹

¹Shenzhen Key Laboratory for Systems Medicine in Inflammatory Diseases, School of Medicine, Shenzhen Campus of Sun Yat-Sen University, Sun Yat-Sen University, Shenzhen, Guangdong, China.

|May 21, 2024

概括

工程 Vesicles 提供编程细胞死亡配体 1 (PD-L1) 和 galectin-9 (Gal-9) 在小鼠中逆转了1型糖尿病. 这些人造细胞外囊泡 (aEVs) 减少了有害的T细胞,并保留了产生胰岛素的β细胞.

科学领域:

免疫学免疫学免疫学
内分泌学在内分泌学.
生物技术是生物技术.

背景情况:

1型糖尿病 (T1D) 的发展涉及降低的免疫检查点连接体,编程细胞死亡连接体1 (PD-L1) 和甲蛋白-9 (Gal-9),在β细胞中.
用PD-L1或Gal-9调节胰腺透T淋巴细胞为新发病的T1D提供了一种治疗策略.

研究的目的:

为了设计人工细胞外囊泡 (aEVs) 过度表达PD-L1和Gal-9,以治疗新发型T1D.
在小鼠模型中研究PD-L1-Gal-9 aEVs对T细胞的免疫调节作用及其治疗潜力.

主要方法:

基因工程巨细胞产生aEVs过度表达PD-L1和Gal-9.
通过PD-1/PD-L1和TIM-3/Gal-9通路评估了aEs与T细胞的相互作用.
在实验室对效应T细胞亡和调控T (Treg) 细胞诱导的评估.
向新发型T1D的非肥胖糖尿病 (NOD) 小鼠服用aEVs.

主要成果:

过度表达Gal-9诱导了具有免疫抑制性质的M2巨细胞两极分化.
在体外,PD-L1-Gal-9 aEVs对T细胞表现出良好的粘附性,并促进了T细胞的效应细胞亡和Treg形成.
在NOD小鼠中,PD-L1-Gal-9 aEVs有效逆转了高血糖症,防止了T1D的进展,并保留了剩余的β细胞.
在接受治疗的小鼠中观察到胰腺CD4+和CD8+T细胞的透和激活减少.

结论:

工程 PD-L1-Gal-9 aEVs 代表了一个有前途的治疗方法,用于新发病的 T1D.
这些aEVs调节T细胞的反应,并通过恢复免疫平衡来保护β细胞.
该研究强调了细胞衍生的aEVs作为针对性传递载体的潜力,用于自身免疫性疾病治疗.

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