Identification of Tim-3 Expression in Acute Myeloid Leukemia: Its Clinical and Laboratory Correlation

Abstract

nderstanding the immune biology of AML and designing rational approaches to target the immune environment to improve outcomes is an area of intense research in AML. Inhibitory checkpoints are part of the normal immune system that function to turn off an immune response. Research on the immune microenvironment of AML has revealed that leukemia cells manipulate the immune system by a dynamic process, through which it takes advantage of the normal inhibitory checkpoints, thus resulting in T-cell exhaustion, a process of gradual loss of T-cell function and down regulation of the immune system. This concept may potentially explain immune escape by hematological malignancies TIM-3 is a type 1cell surface glycoprotein that belongs to TIMs family. TIM-3 is a negative regulatory receptor that plays a vital role in immune suppression in both innate and adaptive immune systems. TIM-3 and its ligand, Gal-9, are expressed on AML blast and LSCs. The Tim-3/Gal-9 autocrine loop plays a key role in the self-renewal of LSCs and the maintenance of AML. Previous studies have investigated the prognostic significance of TIM3 in AML, however the results remained controversial. This prompted us to investigate TIM-3 expression in patients with AML and explore the impact of its expression on the clinico-laboratory characteristics and prognostic behavior of denovo-AML patients.