Hypothesis: Tim-3/galectin-9, a new pathway for leukemia stem cells survival by promoting expansion of myeloid-derived suppressor cells and differentiating into tumor-associated macrophages.

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 mucin-3 (TIM-3), a specific surface molecule expressed on LSCs in most types of AML, is a candidate for AML LSC-targeted therapies. It is important to know how this molecule functions in the maintenance of LSCs and suppression of anti-tumor immunity. Recent data have shown that Tim-3 which expresses on T cells can suppress immune responses indirectly by inducing expansion of myeloid-derived suppressor cells (MDSCs). MDSCs at the leukemia site can also differentiate into tumor-associated 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 Tim-3, 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.

journal_name

Cell Biochem Biophys

authors

Gao L,Yu S,Zhang X

doi

10.1007/s12013-014-9900-0

subject

Has Abstract

pub_date

2014-09-01 00:00:00

pages

273-7

issue

1

eissn

1085-9195

issn

1559-0283

journal_volume

70

pub_type

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