Figure 3.
Immune checkpoint blockade to reinstate the GVL effect. Schematic representation of inhibitory-costimulatory immune receptors, their ligands, and the available monoclonal antibodies (MoAbs) to counteract T-cell inhibition. Upregulation of PD-1, CTLA-4, TIM-3, and TIGIT receptors on T cells (in red) mirrors the immunophenotypic changes observed in leukemic blasts (in violet) ligands because PD-L1/PD-L2, CD80/CD86, B7 molecules, Gal-9, and PVR/PVRL-2 and their interactions are responsible for T-cell impairment. Monoclonal antibodies can be used to block these interactions, either in monotherapy or in combination with HMAs (azacitidine, decitabine), which can potentiate these effects through upregulation of the relevant ligands, HLAs, and of tumor antigens in leukemic cells.

Immune checkpoint blockade to reinstate the GVL effect. Schematic representation of inhibitory-costimulatory immune receptors, their ligands, and the available monoclonal antibodies (MoAbs) to counteract T-cell inhibition. Upregulation of PD-1, CTLA-4, TIM-3, and TIGIT receptors on T cells (in red) mirrors the immunophenotypic changes observed in leukemic blasts (in violet) ligands because PD-L1/PD-L2, CD80/CD86, B7 molecules, Gal-9, and PVR/PVRL-2 and their interactions are responsible for T-cell impairment. Monoclonal antibodies can be used to block these interactions, either in monotherapy or in combination with HMAs (azacitidine, decitabine), which can potentiate these effects through upregulation of the relevant ligands, HLAs, and of tumor antigens in leukemic cells.

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