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Updated: Jun 12, 2025

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通过JAK2/STAT3通路,CXCR4调节了通过TOX编程的CD8+ T细胞的耗尽表型

Canhui Cao1, Miaochun Xu2, Ye Wei1

  • 1Department of Gynecologic Oncology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China; Cancer Biology Research Center (Key Laboratory of the Ministry of Education), Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430199, China; Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China; National Clinical Research Center for Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.

Cell genomics
|September 24, 2024
PubMed
概括

CXCR4抗剂可以改善癌症免疫疗法. 这项研究揭示了CXCR4驱动T细胞疲劳,并阻止它恢复免疫功能,支持组合疗法.

关键词:
CD8 T 细胞 CD8 T 细胞CXCR4CXCR4CXCR4CXCR4CXCR4CXCR4CXCR4CXCR4CXCR4CXCR4C通过JAK2-STAT3路径.在PD-1中使用PD-1.T细胞耗尽的情况免疫检查点封锁封锁免疫疗法 免疫疗法一个单细胞的ATAC-seqq.一个单细胞RNA-seqq.瘤微环境是一个微环境.

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