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一点"BiTS"的LAG3激动性,对T细胞自身免疫力有很大的影响

Qianqian Ming¹, Vincent C Luca¹

¹Department of Immunology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, 33612, USA.

Immunology and cell biology

|November 2, 2025

概括

免疫检查点蛋白LAG3 (淋巴细胞激活基因3) 通过形成凝结物来抑制T细胞激活. 一个新的BiTS分子通过将LAG3与T细胞受体 (TCR) 结合来模仿这种情况.

科学领域:

免疫学免疫学免疫学
分子生物学分子生物学
细胞生物学细胞生物学

背景情况:

淋巴细胞激活基因3 (LAG3) 是一种免疫检查点受体,在T细胞调节中发挥作用.
LAG3与MHC II类 (MHC-II) 分子结合,导致抑制T细胞激活.
这种抑制是由免疫突触中的蛋白质-蛋白质相互作用和分子凝聚物的形成介导的.

研究的目的:

研究LAG3与MHC-II结合抑制T细胞激活的分子机制.
探索凝结物形成在LAG3介导的T细胞抑制中的作用.
设计和评估一种模仿MHC-II在LAG3参与中的新型分子.

主要方法:

使用生物化学分析来研究LAG3和CD3ε之间的蛋白质-蛋白质相互作用.
采用先进的显微镜技术,可视化免疫突触的凝结物形成.
设计了一种双特异性绑定分子 (BiTS),以模仿MHC-II与LAG3.3的结合.

主要成果:

证明了LAG3-MHC-II结合会诱导LAG3和CD3ε细胞内域之间的凝析物形成.
表明这些凝结物对于抑制T细胞激活至关重要.
证实工程BiTS分子成功地重复了MHC-II诱导的结合和凝结形成,导致T细胞抑制.

结论:

通过LAG3介导的T细胞抑制取决于特定细胞内凝聚物的形成.
BiTS分子是研究LAG3功能和潜在开发新型免疫疗法的宝贵工具.
针对LAG3-CD3ε相互作用提供了一个有希望的策略,用于调节癌症和自身免疫性疾病中的免疫反应.

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