1404-恢复CD226表达以克服HER2+乳腺癌TIGIT耐药免疫

这项研究探讨了HER2+乳腺癌对常规治疗产生抗性的免疫机制，并提出了一种新型联合免疫疗法。研究发现，肿瘤细胞通过CD112/CD155配体激活CD8+ T细胞上的抑制性受体TIGIT，从而诱导免疫逃逸。通过将抗TIGIT抗体与抗HER2治疗结合，可以重新激活T细胞中由TBX21驱动的CD226共刺激信号，进而增强干扰素释放并消除耐药肿瘤亚群。实验证明，CD8+CD226+ T细胞的浸润密度是预测该疗法疗效及患者生存预后的关键生物标志物。该研究为攻克HER2+乳腺癌的耐药性提供了重要理论依据。References:Zhang L, Li J, Xiu B, et al. Restoring the CD226 in CD8+ T cells overcomes TIGIT-refractory immunity in HER2+ breast cancer[J]. Cell Death & Disease, 2026.前往小宇宙评论区与主播互动

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1404-恢复CD226表达以克服HER2+乳腺癌TIGIT耐药免疫

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