和信号转导和转录激活蛋白3(Stat3)的双重调节剂与针对程序性细胞死亡1(PD1)蛋白的抗体,抗程序性细胞死亡蛋白1配体(PDL1)抗体或其组合的组合.通过增强肿瘤对所述抗PD1和/或抗PDL1抗体的响应,将非响应性肿瘤转变成响应性肿瘤和/或阻断肿瘤进展,所述组合可用于使可能发展出或已发展出对所述抗PD1和/或抗PDL1抗体...
[1]. Tang J, Yu JX, Hubbard-Lucey VM, Neftelinov ST, Hodge JP, Lin Y. Trial watch: The clinical trial landscape for PD1/PDL1 immune checkpoint inhibitors. Nat Rev Drug Discov. 2018;17(12):854-855. doi:10....
4a–d). These results above indicate that, in the HCC environment, neutrophils are activated by fibroblast-derived soluble factors and acquire the ability to suppress T-cell function through the PD1/PDL1 pathway. Fig. 4 HCC-CAF-primed neutrophils suppress T-cell immunity through the STAT3-PDL1...
4F-G). There were significantly increased cells expressing checkpoint protein PDL1 (p = 0.0087) but not PD1 (p = 0.1744) (Fig. 4H-I). The % of Ki67 + tumor cells was significantly lower in tumors with high pSTAT3 (p = 0.0002) (Fig. 4J). Fig. 4 Immune and ...
[1]. Tang J, Yu JX, Hubbard-Lucey VM, Neftelinov ST, Hodge JP, Lin Y. Trial watch: The clinical trial landscape for PD1/PDL1 immune checkpoint inhibitors. Nat Rev Drug Discov. 2018;17(12):854-855. doi:10.1038/nrd.2018.210
本发明提供了AKT/STAT3作为免疫检查点抑制剂的靶点的用途,并提供了AKT/ATAT3抑制剂在制备治疗肿瘤和/或自身免疫性疾病的药物及制备PD1/PDL1抑制剂中的新用途;AKT/ATAT3抑制剂在抑制AKT/STAT3通路活性的同时,能显著抑制PDL1的表达水平,进而阻断PD1与PDL1的结合,使T细胞恢复活性,从而增强T细胞抗肿瘤免疫应答,能抑制...
本发明提供了AKT/STAT3作为免疫检查点抑制剂的靶点的用途,并提供了AKT/ATAT3抑制剂在制备治疗肿瘤和/或自身免疫性疾病的药物及制备PD1/PDL1抑制剂中的新用途;AKT/ATAT3抑制剂在抑制AKT/STAT3通路活性的同时,能显著抑制PDL1的表达水平,进而阻断PD1与PDL1的结合,使T细胞恢复活性,从而增强T细胞抗肿瘤免疫应答,能抑制...
本发明提供了AKT/STAT3作为免疫检查点抑制剂的靶点的用途,并提供了AKT/ATAT3抑制剂在制备治疗肿瘤和/或自身免疫性疾病的药物及制备PD1/PDL1抑制剂中的新用途;AKT/ATAT3抑制剂在抑制AKT/STAT3通路活性的同时,能显著抑制PDL1的表达水平,进而阻断PD1与PDL1的结合,使T细胞恢复活性,从而增强T细胞抗肿瘤免疫应答,能抑制...
However, this interaction is reversible and blockade of PD1/PDL1 interactions restores T-cell function. Accordingly, the PD1/PDL1 signaling axis is often hijacked by cancer cells to evade immune-mediated tumor surveillance, while inhibition of this pathway enhances tumor cell death [282]. Of note...
Besides, silencing of miR-155-5p could initiate the PD1/PDL1 pathway-mediated macrophage M2 polarization and inhibit ITP progression by up-regulating SOCS1 (Chang et al., 2020). Given this background we examined differences in the proportion of M2 phenotype macrophages in ITP patients and ...