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In normal conditions, mutated antigens from tumor cells will lead to the activation of T cells that bind to and trigger apoptosis in target cancer cells. On the surface of T cells are PD-1 (programmed cell death-1) receptors whose ligands include PD-L1 and PD-L2.
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Together, PD-1 and PD-L1/PD-L2 are involved with inhibiting T cell response so that the immune response is only initiated when necessary, avoiding chronic autoimmune inflammation.
However, tumor cells have utilized the PD-1/PD-L1 pathway to resist anticancer immune responses by producing abnormally high levels of PD-L1. When the PD-L1 ligands bind to the PD-1 receptors on T cells, the T cells become deactivated and anti-tumor activity is obstructed.
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