阻断Tim-3/Tim-3L信号途径打破胰腺癌细胞免疫耐受
基本信息
结项摘要
胰腺癌免疫治疗首要屏障是荷瘤机体T细胞对肿瘤的免疫耐受。Tim-3是新发现的仅特异性表达于Th1细胞的膜蛋白，作用为介导Th1细胞的特异性抑制，Tim-3/Tim-3L信号途径在机体免疫耐受诱导中居核心地位。Treg细胞通过其表面Tim-3配体(Tim-3L,Galectin-9)与Th1细胞表面Tim-3作用后负向调控Th1细胞免疫功能，且抑制Th1辅助的幼稚性CD8+T分化与增殖及效应CTL对肿瘤细胞的特异性杀伤，直接参与肿瘤免疫耐受病理过程。我们前期观察到胰腺癌荷瘤机体内Tim-3/Tim-3L 信号途径被过度激活，如果可干扰此信号途径将有助于解除对荷瘤机体T细胞对胰癌细胞的免疫耐受。本项目拟进一步深入探讨Tim-3/Tim-3L信号途径在荷瘤状态下过度激活的机理，并以Tim-3L为干预靶点，采用多种方法，阻断Tim-3/Tim-3L信号途径，观察其打破胰癌细胞诱导免疫耐受的效果。
项目摘要
项目成果
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数据更新时间：2023-05-31
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