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. 2021 Feb 25;11:624742. doi: 10.3389/fonc.2021.624742

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Copyright © 2021 Wong, Hassan and Yaacob

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Synergism of decitabine or guadecitabine with antileikemic immune cells and engineered T cells, and depletion of immunosuppressive cells in AML or MDS microenviroment. (A) DC/AML vacinne combined with decitabine or guadecitabine treatment induces leukemia-specific immunity; (B) Decitabine potentiates infused NK cells’ antileukemia activity by upregulating ligands for NKG2D and DNAM-1 immunoactivating receptors on NK cells. Decitabine combined with anti-CD33 mAb also augments the expression of NKG2D ligands in AML cells; (C) Upregulation of CTA expression such as NY-ESO-1 by decitabine or guadecitabine treatment synergizes with NY-ESO-1 cancer vaccine treatment; (D) Combination of decitabine or guadecitabine with novel immune checkpoint blockade therapy such as anti-TIGIT therapeutic antibody to circumvent resitance of AML or MDS cells to either hypomethylating agent; (E) Potential synergsim of decitabine or guadecitabine with anti-CD123 therapeutic antibody (e.g. tagraxofusp) to induce antileukemic immunity; (F) Decitabine treatment synergizes with CD123 CAR-T cells against AML cells; (G) Potential synergism of decitabine or guadecitabine with WT-1 specific TCR-T cells. ADCC: Antibody-dependent cellular cytotoxicity; AML: Acute myeloid leukemia; CAR-T: Chimeric antigen receptor-engineered T cell; CTA: Cancer/testis antigen; DC: Dendritic cell; DNAM-1: DNAX accessory molecule-1; ICR: Immune checkpoint receptor; ICRL: Immune checkpoint receptor ligand; mAb: Monoclonal antibody; MDS: Myelodysplastic syndromes; MDSC: Myeloid-derived suppressor cell; MHC: Major histocompatibility complex; NK: Natural killer; NKG2D: Natural killer group 2D; TCR: T cell receptor; TCR-T: T cell receptor-engineered T cell; TIGIT: T-cell immunoreceptor with Ig and ITIM domains; WT1: Wilms’ tumor 1. Upward arrow denotes upregulated expression, increased CTA presentation, or induced apoptosis of MDSCs.