Abstract
Acute myeloid leukemia (AML), a malignant disorder of hemopoietic stem cells. AML can escape immunosurveillance of natural killer (NK) by gene mutation, fusions, and epigenetic modification, while the mechanism is not clearly understood. Here we show that the expression of Intercellular adhesion molecule‐1 (ICAM‐1, CD54) is silenced in AML cells. Decitabine could upregulate ICAM-1 expression, which contributes to the NK-AML cell conjugates and helps NK cells kill AML cells. We also show that ICAM-1 high expression can reverse the AML immune evasion and activate NK cells function in vivo. This study suggests that a combination of the hypomethylating agent and NK cell infusion could be a new strategy to cure AML.
Highlights
AML is a heterogeneous disease from the biological and clinical standpoint with increasing incidence, high mortality, and a very poor prognosis [1, 2]
Studies showed that promoting the NK-AML cell conjugate formation by upregulating lymphocyte-function associated (LFA) antigen expression on NK cells and by inducing ICAM-1 expression on AML cells could increase their cytotoxic activities [7]
To determine the role of ICAM-1 in the AML patients, ICAM-1 mRNA expression was analyzed in the bone marrow or peripheral blood of 70 healthy controls and 173 AML patients from The Cancer Genome Atlas (TCGA) by GEPIA [16, 17]
Summary
AML is a heterogeneous disease from the biological and clinical standpoint with increasing incidence, high mortality, and a very poor prognosis [1, 2]. Immunotherapy with strategies aimed at boosting the immune response has pushed NKs into the spotlight [2]. Studies showed that promoting the NK-AML cell conjugate formation by upregulating lymphocyte-function associated (LFA) antigen expression on NK cells and by inducing ICAM-1 expression on AML cells could increase their cytotoxic activities [7]. Restoring ICAM-1 expression in AML may combine the benefit of targeting AML cells and NK-mediated killing. Limited studies are relating to how to increase the ICAM-1 expression on the surface of AML cells
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