Abstract
Programmed death ligand-1 (PDL-1) is an immune regulatory component that is expressed on normal cells, tumor cells, and non-tumor immune cells. The expression of these checkpoint components on the cell surface helps prevent the immune system's overactivity. PDL-1 is associated with immune evasion in many solid tumors and lymphomas, while its clinical signicance is under exploration in leukemias. Structural and regulatory aspects are recently presented in reports that dene the role of signaling components in regulating PDL-1. Immune interactions of soluble cytokines such as IFN-γ & TNF-α with PDL1 show relevance in liquid malignancies. Recent reports have shown that interaction occurs between IFN- γ and PDL 1, but the exact mechanism is not dened. PDL1 expression around 20-25% across the malignancies has put this immune checkpoint in clinical trials, and many solid malignancies have shown better clinical outcomes and survival rates. Still, resistance remains a signicant hurdle. Immune resistance is the primary reason for the minimal impact of PDL-1 blockade therapy in various cancers. IFN-γ induced PDL1 immunotherapy could be effective in leukemias to overcome the resistance and provide effective immune responses and overall better clinical outcomes.
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