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Updated: Sep 9, 2025

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腫瘍由来のEBI3は,胃がんにおけるSTAT4-IL-10/CCL5経由によるCD8+T細胞枯渇を促進する

Yong-Jia Yan1, Xin Liu1, Daohan Wang1

  • 1Tianjin Medical University General Hospital, Tianjin, China.

Cancer immunology research
|September 1, 2025
PubMed
まとめ

エピジェネティックレギュレータEBI3は,胃がん (GC) のT細胞枯渇を促進し,免疫療法を阻害する. 抗EBI3ペプチドが開発され,この疲労を逆転させ,GC患者にとって新しい治療戦略を提供しました.

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