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Programmed cell death-1 and its ligands: Current knowledge and possibilities in immunotherapy.
- Source :
-
Clinics (Sao Paulo, Brazil) [Clinics (Sao Paulo)] 2023 Mar 14; Vol. 78, pp. 100177. Date of Electronic Publication: 2023 Mar 14 (Print Publication: 2023). - Publication Year :
- 2023
-
Abstract
- Programmed Cell Death-1 (PCD-1) is a key immune checkpoint receptor, which mainly expresses on activated T, B, Dendritic (DC), Natural Killer (NK), and Treg cells. On the surface of activated T-cells, PCD-1 expression is upregulated after the recognition of peripherals antigens by T cells; subsequently, the elevated binding of PD-1 to Programmed Death Ligand-1 (PD-L1) and Programmed Death Ligand-2 (PD-L2) becomes a key step for downstream inhibitory signaling. Although the role of PD-L1 has been evaluated more thoroughly by clinical research, and PD-L1 has also been used more widely in the clinical setting, PD-L2 also plays an important role in the negative regulation of T-cells, one of the necessary conditions that lead to immune tolerance. Expression of PD-L1 either in tumors or in infiltrating immune cells has been verified predominantly by Immunohistochemistry (IHC) in a variety of tumors, suggesting a role for the PD-1/PD-L1 axis as a prognostic trait and therapeutic target across multiple histotypes. The complex interplay between these factors plays a major role in the diffusion and clinical application of PD-L1 IHC assays as predictive biomarkers of response to PD-1/PD-L1 inhibitors. Checkpoint blockades are registered for the treatment of various cancers, including gynecological malignancies.<br />Competing Interests: Conflicts of interest The authors declare no conflicts of interest.<br /> (Copyright © 2023 HCFMUSP. Published by Elsevier España, S.L.U. All rights reserved.)
Details
- Language :
- English
- ISSN :
- 1980-5322
- Volume :
- 78
- Database :
- MEDLINE
- Journal :
- Clinics (Sao Paulo, Brazil)
- Publication Type :
- Academic Journal
- Accession number :
- 36931099
- Full Text :
- https://doi.org/10.1016/j.clinsp.2023.100177