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基新抗原免疫原性的分子机制

Yury Patskovsky^1,2, Aswin Natarajan^1,2, Larysa Patskovska^1,2

¹Department of Pathology, New York University Grossman School of Medicine, New York, NY, USA.

Nature communications

|June 23, 2023

概括

改变的蛋白质酸化会产生癌症声抗原. 一个T细胞受体 (TCR27) 和一种急性髓性白血病基抗原 (pMLL) 之间的特定相互作用揭示了癌症免疫治疗的关键结合机制.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
结构生物学结构生物学

背景情况:

癌细胞中改变的蛋白质酸化可以产生光新抗原.
这些新抗原在癌症免疫性中的确切作用尚未完全理解.
了解这些相互作用是开发新型癌症免疫疗法的关键.

研究的目的:

阐明一种特定的急性髓性白血病基抗原被T细胞受体识别的机制.
为了研究基抗原与T细胞受体之间的相互作用的结构基础.
探索这种相互作用对癌症免疫疗法开发的潜力.

主要方法:

进行X射线晶体学以确定TCR27和脂-MHC复合物的结构.
核磁共振 (NMR) 用于绘制TCR27和MHC-类之间的接口.
信息驱动的蛋白质对接生成一个三元复杂模型.

主要成果:

该研究确定了一种特定的基抗原,pMLL747-755,被T细胞受体TCR27.7识别.
结构和结合分析显示,涉及表位的酸盐组的非共价相互作用对TCR特异性至关重要.
对素残留物的修改影响了T细胞激活和TCR-pMHC结合,尽管保持了pMHC的构型和亲和力.

结论:

基抗原的酸盐组在TCR27.27的特定识别中起着至关重要的作用.
这种对TCR-pMHC相互作用的详细理解可以指导针对癌症免疫治疗的T细胞受体的优化.
这些发现支持扩大治疗点和优化T细胞受体,以改善癌症治疗选择.

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