In PD1 resistant mouse tumor models, deletion of CD155 prevented accumulation of intratumor PD1hiCD8+ T cells. Additionally, therapeutic blockade of the CD155 cognate receptors TIGIT and CD96 restored IFN纬 production and improved anti-PD1 tumor control. Conclusion Our findings are the first to ...
Combination of 4-1BB agonist and PD-1 antagonist promotes antitumor effector/memory CD8 T cells in a poorly immunogenic tumor model. Cancer Immunol. Res. 3, 149–160 (2015). Article CAS PubMed Google Scholar Woo, S. R. et al. Immune inhibitory molecules LAG-3 and PD-1 synergistically...
Combination of PD1 Inhibitor and OX40 Agonist Induces Tumor Rejection and Immune Memory in Mouse Models of Pancreatic Cancer 来自 国家科技图书文献中心 喜欢 0 阅读量: 129 作者:Y Ma,J Li,H Wang,Y Chiu,C Yee 摘要: Background Aims Advanced pancreatic ductal adenocarcinoma (PDAC) is resistant to...
In principle, no fewer than 20 patients were included per tumor type, and the number of patients enrolled with each tumor type was adjusted in a timely manner based on the efficacy and safety results found during the research. The primary objective of phase Ib was to evaluate the preliminary...
et al. Mechanism of tumor rejection with doublets of CTLA-4, PD-1/PD-L1, or IDO blockade involves restored IL-2 production and proliferation of CD8+ T cells directly within the tumor microenvironment. J. Immunother. Cancer 2, 3 (2014). PubMed PubMed Central Google Scholar Juneja, V....
(12). In contrast, T cells recognize MHC-presented peptides derived from shared tumor antigens or neoantigens created by somatic mutations (2). Therefore, tumors resistant to cytotoxic T cells may respond to NK cell–based immunotherapies. In fact, loss of MHC-I expression by tumor cells ...
Abstract Patients with metastatic HER2 breast cancer (MBC) often become resistant to HER 2 targeted therapy and have recurrence of disease. The Panacea trial suggested that HER2 MBC patients were more likely to respond to checkpoint therapy if TIL were present or if tumor expressed PD-L1. We as...
[40]. Here, we suggest that exosome-derived circCCAR1 is taken in by CD8 + T cells, which further increases the stability of PD1, causes CD8 + T-cell exhaustion and leads to tumor immunosuppression. Notably, HCC cells with high circCCAR1 expression were resistant to anti-PD1 ...
[0260] Fumet ,Jean‑David ,Corentin Richard ,Fanny Ledys ,Quentin Klopfenstein , Philippe Joubert,Bertrand Routy ,Caroline Truntzer等人 ,2018.Prognostic and Predictive Role of CD8 and PD‑L1Determination in Lung Tumor Tissue of Patients under Anti‑PD‑1Therapy .British Journal of Cancer ...
hyperexpression of FSTL3 could prompt the resistance of mouse tumors to anti-PD1 therapy. This study reveals the exact role of FSTL3 in immune evasion and ICB therapy resistance in CRC, which is essential for finding a new biomarker and therapeutic pathway for those CRC patients resistant to ...