Journal
MOLECULAR CELL
Volume 76, Issue 3, Pages 359-370Publisher
CELL PRESS
DOI: 10.1016/j.molcel.2019.09.030
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Funding
- Cancer Prevention & Research Institute of Texas (MIRA) [RP160710]
- NIH [R01 AI116722]
- National Breast Cancer Foundation
- Breast Cancer Research Foundation [BCRF-17069]
- Patel Memorial Breast Cancer Endowment Fund
- University of Texas MD Anderson-China Medical University Sister Institution Fund
- Inha University Institution Fund
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The engagement of programmed cell death protein 1 (PD-1; encoded by the PDCD1 gene) receptor expressed on activated T cells and its ligand, programmed death-ligand 1 (PD-L1; encoded by the CD274 gene), is a major co-inhibitory checkpoint signaling that controls T cell activities. Various types of cancers express high levels of PD-L1 and exploit PD-L1/PD-1 signaling to evade T cell immunity. Blocking the PD-L1/PD-1 pathway has consistently shown remarkable anti-tumor effects in patients with advanced cancers and is recognized as the gold standard for developing new immune checkpoint blockade (ICB) and combination therapies. However, the response rates of anti-PD-L1 have been limited in several solid tumors. Therefore, furthering our understanding of the regulatory mechanisms of PD-L1 can bring substantial benefits to patients with cancer by improving the efficacy of current PD-L1/PD-1 blockade or other ICBs. In this review, we provide current knowledge of PD-L1 regulatory mechanisms at the transcriptional, post-transcriptional, post-translational, and extracellular levels, and discuss the implications of these findings in cancer diagnosis and immunotherapy.
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