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The E3 ubiquitin ligase TRAF6 controls CTLA-4 turnover and promotes T-cell-mediated antitumor immunity

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摘要 Yu et al.[1]reported that the tumor necrosis factor(TNF)receptor OX40(CD134)-TNF receptor-associated factor 6(TRAF6)axis mediates Lys63-linked ubiquitination and subsequent lysosomal degradation of cytotoxic T-lymphocyte antigen 4(CTLA-4),leading to the enhancement of CD8^(+)T-cell-mediated antitumor immunity.Their findings unveil a previously unknown mechanism in controlling the stability of the immune checkpoint CTLA-4 and provide a potential therapeutic target for the improvement of Tcell-based immunotherapy.
出处 《Cellular & Molecular Immunology》 SCIE CAS CSCD 2024年第1期97-99,共3页 中国免疫学杂志(英文版)
基金 funded by the Key Project of the National Natural Science Foundation of China(81830093) the Non-Profit Central Research Institute Fund of CAMS(2022-RC310-05,2021-RC310-003,2020-RC310-002) CAMS Initiative for Innovative Medicine(2022-I2M-2-001) the National Natural Science Foundation of China(82372944).
关键词 immunity OX40 UBIQUITIN
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