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Review
. 2021 Feb 10;39(5):419-432.
doi: 10.1200/JCO.20.00475. Epub 2021 Jan 12.

Immune Biology of Acute Myeloid Leukemia: Implications for Immunotherapy

Sophia Khaldoyanidi  1 , Dirk Nagorsen  1 , Anthony Stein  2 , Gerrit Ossenkoppele  3 , Marion Subklewe  4
Affiliations
Review

Immune Biology of Acute Myeloid Leukemia: Implications for Immunotherapy

Sophia Khaldoyanidi et al. J Clin Oncol. .
No abstract available

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Figures

FIG 1.
FIG 1.
Cellular and molecular mechanisms of immune evasion in acute myeloid leukemia (AML) in the vascular and bone marrow microenvironments., Cells that inhibit anti-AML immune function include regulatory T cells (Tregs), myeloid-derived suppressor cell (MDSCs), and mesenchymal stromal cells (MSCs). On the molecular level, activation of immune checkpoint pathways (eg, programmed death receptor-1 [PD-1], cytotoxic T-lymphocyte–associated protein 4 [CTLA-4]) and induction of immunosuppressive soluble factors (eg, kynurenine) by AML tumor microenvironment (TME) interactions fosters immune escape in AML. Additionally, under the pressure of allogeneic T cells, immuno-editing driven by epigenetic mechanisms may result in downregulation of major histocompatibility complex (MHC) expression on AML cells, leading to immune escape and relapse in AML. ATP, adenosine triphosphate; CCR4, C-C chemokine receptor type 4; GAL9, galectin-9; IDO, indoleamine-2,3 dioxygenase; IFN-γ, interferon gamma; IL, interleukin; iNOS, inducible nitric oxide synthase; LSC, leukemic stem cell; MPS, metalloproteinases; NK, natural killer; NOS-2, nitric oxide synthase 2; ROS, reactive oxygen species; SDF1, stromal cell-derived factor 1; SIRPα, signal regulatory protein alpha; TCR, T-cell receptor; TGFβ, transforming growth factor beta; TIM-3, T-cell immunoglobulin and mucin-domain containing-3; VEGF, vascular endothelial growth factor; VISTA, V-domain immunoglobulin suppressor of T-cell activation.
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