Authors: Lei Gao Shicang Yu Xi Zhang
Publish Date: 2014/03/18
Volume: 70, Issue: 1, Pages: 273-277
Abstract
Despite the improvements in chemotherapy about 60 of acute myeloid leukemia AML remission patients still relapse Leukemic stem cells LSCs are the main causes for the relapse and refractory T cell immunoglobulin mucin3 TIM3 a specific surface molecule expressed on LSCs in most types of AML is a candidate for AML LSCtargeted therapies It is important to know how this molecule functions in the maintenance of LSCs and suppression of antitumor immunity Recent data have shown that Tim3 which expresses on T cells can suppress immune responses indirectly by inducing expansion of myeloidderived suppressor cells MDSCs MDSCs at the leukemia site can also differentiate into tumorassociated macrophages TAMs TAMs can promote proliferation and survival of LSCs by the diversion of adaptive immunity and the facilitation of extracellular matrix remodeling angiogenesis and lymphangiogenesis Our previous study in AML patient bone marrow samples showed CD68+ macrophages around AML clone Based on the known evidence and our experimental findings we hypothesize that Tim3 which specifically expresses on LSCs is beneficial for LSCs survival and AML progression by promoting expansion of MDSCs and differentiating into TAMs at the leukemia site
Keywords: