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<p>Activating the type I interferon response in tumor cells and enhancing T cell-mediated anti-tumor immunity have broad clinical applications in tumor immunotherapy. However, the detailed mechanisms underlying the antitumor immune response and type I interferon response in nasopharyngeal carcinoma (NPC) remain unclear and require further elucidation. In this study, we identify CD38 in NPC cells as a key mediator impairing T cell antitumor immunity. Mechanistically, CD38 induces mitochondrial autophagy through PHB2, enhances the interaction between PHB2 and MAVS, leading to the degradation of MAVS protein, and inhibits the type I interferon response and CD8<sup>+</sup>T cell-mediated anti-tumor immunity. Importantly, CD38 promotes tumor progression and reduces the proportion of CD8<sup>+</sup>T cells and IFNγ<sup>+</sup>CD8<sup>+</sup>T cells in vivo via MAVS. In conclusion, these findings reveal previously unrecognized roles and mechanisms of CD38 in regulating anti-tumor T cell immunity, suggesting that inhibition of CD38 could initiate tumor-targeted immune responses, enhance anti-tumor immunity in patients, and provide new therapeutic strategies for NPC.</p>

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CD38 degrades MAVS through mitophagy to inhibit type I interferon secretion in nasopharyngeal carcinoma cells and impairs CD8+T cell-mediated anti-tumor immunity

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月9日

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  • Lin Liang,
  • Wentao Li,
  • Siyi Liu,
  • Qian He,
  • Feng Zeng,
  • Jiaying Cao,
  • Yan Lei,
  • Yanling Li,
  • Yanhong Zhou

摘要

Activating the type I interferon response in tumor cells and enhancing T cell-mediated anti-tumor immunity have broad clinical applications in tumor immunotherapy. However, the detailed mechanisms underlying the antitumor immune response and type I interferon response in nasopharyngeal carcinoma (NPC) remain unclear and require further elucidation. In this study, we identify CD38 in NPC cells as a key mediator impairing T cell antitumor immunity. Mechanistically, CD38 induces mitochondrial autophagy through PHB2, enhances the interaction between PHB2 and MAVS, leading to the degradation of MAVS protein, and inhibits the type I interferon response and CD8+T cell-mediated anti-tumor immunity. Importantly, CD38 promotes tumor progression and reduces the proportion of CD8+T cells and IFNγ+CD8+T cells in vivo via MAVS. In conclusion, these findings reveal previously unrecognized roles and mechanisms of CD38 in regulating anti-tumor T cell immunity, suggesting that inhibition of CD38 could initiate tumor-targeted immune responses, enhance anti-tumor immunity in patients, and provide new therapeutic strategies for NPC.