Open AccessAcute myeloid leukemia immune escape by epigenetic CD48 silencing
Author(s) -
Zhiding Wang,
Yang Xiao,
Wei Guan,
Mengzhen Wang,
Jinghong Chen,
Linlin Zhang,
Yan Li,
Qian Xiong,
Hong Wang,
Maoquan Wang,
Yuyan Li,
Na Lv,
Yonghui Li,
Lixin Wang,
Li Yu
Publication year - 2020
Publication title -
clinical science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.91
H-Index - 138
eISSN - 1470-8736
pISSN - 0143-5221
DOI - 10.1042/cs20191170
Subject(s) - myeloid leukemia , hypomethylating agent , immunosurveillance , epigenetics , immune system , biology , cancer research , leukemia , myeloid , haematopoiesis , gene silencing , immunology , dna methylation , stem cell , gene expression , microbiology and biotechnology , gene , genetics
Acute myeloid leukemia (AML) is a malignant disorder of hemopoietic stem cells. AML can escape immunosurveillance of natural killer (NK) by gene mutation, fusions and epigenetic modification. The mechanism of AML immune evasion is not clearly understood. Here we show that CD48 high expression is a favorable prognosis factor that is down-regulated in AML patients, which can help AML evade from NK cell recognition and killing. Furthermore, we demonstrate that CD48 expression is regulated by methylation and that a hypomethylating agent can increase the CD48 expression, which increases the NK cells killing in vitro. Finally, we show that CD48 high expression can reverse the AML immune evasion and activate NK cells function in vivo. The present study suggests that a combination the hypomethylating agent and NK cell infusion could be a new strategy to cure AML.