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. 2021 Jul 23;36(1):13–22. doi: 10.1038/s41375-021-01350-x

Fig. 1. AML blast’s immune escaping strategies.

Fig. 1

Schematic illustration summarizing the most known immune evasion mechanisms exerted by AML blasts. AML blasts can hamper T- and NK-cell effector functions by aberrantly overexpressing inhibitory T-cell ligands (i.e. PD-L1, Gal-9, CD155, CD112, CD86) (1), or by releasing soluble forms of NKG2DL (2). AML blasts promote T-cell exhaustion and apoptosis, drive the expansion of regulatory T cells (Tregs) and myeloid-derived suppressor cells (MDSCs), and induce the switch of macrophages to tumor-associated macrophages (TAMs) (3) by altering the cytokine milieu and through the release within the BM niche of other soluble factors such as reactive oxygen species (ROS), indoleamine 2,3-dioxygenase-1 (IDO1), arginase II (ArgII), and extracellular vesicles (EVs) (4). Moreover, AML blasts reduce their expression of antigen presentation molecules, thus hiding themselves from immune cells such as dendritic cells (DCs) and macrophages (5). Figure created with Biorender.