Revisiting the PD-1 pathway
Programmed Death-1 (PD-1; CD279) is an inhibitory receptor induced in activated T cells.
PD-1 engagement by its ligands, PD-L1 and PD-L2, maintains peripheral tolerance but also …
PD-1 engagement by its ligands, PD-L1 and PD-L2, maintains peripheral tolerance but also …
Insights from a 30-year journey: function, regulation and therapeutic modulation of PD1
K Chamoto, T Yaguchi, M Tajima, T Honjo - Nature Reviews …, 2023 - nature.com
PD1 was originally discovered in 1992 as a molecule associated with activation-induced cell
death in T cells. Over the past 30 years, it was found that PD1 has a critical role in avoiding …
death in T cells. Over the past 30 years, it was found that PD1 has a critical role in avoiding …
[HTML][HTML] Proteogenomic characterization reveals therapeutic vulnerabilities in lung adenocarcinoma
To explore the biology of lung adenocarcinoma (LUAD) and identify new therapeutic
opportunities, we performed comprehensive proteogenomic characterization of 110 tumors …
opportunities, we performed comprehensive proteogenomic characterization of 110 tumors …
Androgen conspires with the CD8+ T cell exhaustion program and contributes to sex bias in cancer
Sex bias exists in the development and progression of nonreproductive organ cancers, but
the underlying mechanisms are enigmatic. Studies so far have focused largely on sexual …
the underlying mechanisms are enigmatic. Studies so far have focused largely on sexual …
[HTML][HTML] LAG-3: from molecular functions to clinical applications
T Maruhashi, D Sugiura, I Okazaki… - … for immunotherapy of …, 2020 - ncbi.nlm.nih.gov
To prevent the destruction of tissues owing to excessive and/or inappropriate immune
responses, immune cells are under strict check by various regulatory mechanisms at …
responses, immune cells are under strict check by various regulatory mechanisms at …
Efficacy and safety of pembrolizumab in previously treated advanced cervical cancer: results from the phase II KEYNOTE-158 study
HC Chung, W Ros, JP Delord, R Perets… - Journal of Clinical …, 2019 - ascopubs.org
PURPOSE KEYNOTE-158 (ClinicalTrials. gov identifier: NCT02628067) is a phase II basket
study investigating the antitumor activity and safety of pembrolizumab in multiple cancer …
study investigating the antitumor activity and safety of pembrolizumab in multiple cancer …
In vivo molecular imaging for immunotherapy using ultra-bright near-infrared-IIb rare-earth nanoparticles
The near-infrared-IIb (NIR-IIb)(1,500–1,700 nm) window is ideal for deep-tissue optical
imaging in mammals, but lacks bright and biocompatible probes. Here, we developed …
imaging in mammals, but lacks bright and biocompatible probes. Here, we developed …
[HTML][HTML] Anti-NKG2A mAb is a checkpoint inhibitor that promotes anti-tumor immunity by unleashing both T and NK cells
P André, C Denis, C Soulas, C Bourbon-Caillet… - Cell, 2018 - cell.com
Checkpoint inhibitors have revolutionized cancer treatment. However, only a minority of
patients respond to these immunotherapies. Here, we report that blocking the inhibitory …
patients respond to these immunotherapies. Here, we report that blocking the inhibitory …
Roles of PD-1/PD-L1 pathway: signaling, cancer, and beyond
L Ai, A Xu, J Xu - Regulation of Cancer Immune Checkpoints: Molecular …, 2020 - Springer
Immunotherapies that target PD-1/PD-L1 axis have shown unprecedented success in a wide
variety of human cancers. PD-1 is one of the key coinhibitory receptors expressed on T cells …
variety of human cancers. PD-1 is one of the key coinhibitory receptors expressed on T cells …
[HTML][HTML] Binding of LAG-3 to stable peptide-MHC class II limits T cell function and suppresses autoimmunity and anti-cancer immunity
T Maruhashi, D Sugiura, I Okazaki, K Shimizu… - Immunity, 2022 - cell.com
Summary Lymphocyte activation gene-3 (LAG-3) is a potent inhibitory co-receptor; yet, its
functional ligand remains elusive, with distinct potential ligands identified. Here, we …
functional ligand remains elusive, with distinct potential ligands identified. Here, we …