<br>NK 细胞中的 SIRPα-CD47 免疫检查点,Journal of Experimental Medicine

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NK 细胞中的 SIRPα-CD47 免疫检查点
Journal of Experimental Medicine ( IF 12.6 ) Pub Date : 2021-01-08 , DOI: 10.1084/jem.20200839
Tobias Deuse ₁ , Xiaomeng Hu _{1,

2} , Sean Agbor-Enoh _{3,

4} , Moon K Jang ₄ , Malik Alawi ₅ , Ceren Saygi ₅ , Alessia Gravina ₁ , Grigol Tediashvili ₁ , Vinh Q Nguyen ₆ , Yuan Liu ₇ , Hannah Valantine _{8,

9} , Lewis L Lanier ₁₀ , Sonja Schrepfer _{1,

2}

Affiliation

Department of Surgery, Division of Cardiothoracic Surgery, Transplant and Stem Cell Immunobiology Lab, University of California, San Francisco, San Francisco, CA.
Sana Biotechnology, Inc., South San Francisco, CA.
Division of Pulmonary and Critical Care Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD.
Laboratory of Applied Precision Omics, Division of Intramural Research, National Heart, Lung, and Blood Institute, Bethesda, MD.
Bioinformatics Core, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Department of Surgery, University of California, San Francisco, San Francisco, CA.
Department of Biology, Georgia State University, Atlanta, GA.
Division of Cardiovascular Medicine, Stanford University, Stanford, CA.
Laboratory of Transplant Genomics, National Heart, Lung, and Blood Institute, Bethesda, MD.
Department of Microbiology and Immunology, Parker Institute for Cancer Immunotherapy, University of California, San Francisco, San Francisco, CA.

在这里，我们报告了 NK 细胞中免疫检查点信号调节蛋白 α (SIRPα) 的存在和功能，并描述了如何调节它以进行细胞治疗。 NK 细胞 SIRPα 在 IL-2 刺激下上调，以阈值依赖性方式与靶细胞 CD47 相互作用，并对抗其他刺激信号，包括 IL-2、CD16 或 NKG2D。 CD47 表达升高可保护 K562 肿瘤细胞以及小鼠和人类 MHC I 类缺陷靶细胞对抗 SIRPα ⁺原代 NK 细胞，但不能对抗 SIRPα ^- NKL 或 NK92 细胞。 SIRPα 缺陷或抗体阻断增加了 NK 细胞的杀伤能力。人类 MHC 缺陷细胞中恒河猴 CD47 的过度表达可防止异种环境中恒河猴 NK 细胞的细胞毒性。 SIRPα-CD47 轴被发现具有高度物种特异性。总之，结果表明，SIRPα-CD47 免疫检查点的破坏可能会增强 NK 细胞的抗肿瘤反应，并且 CD47 表达的升高可能会阻止 NK 细胞介导的同种异体和异种组织杀伤。

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更新日期：2021-01-10

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