Research Papers:

Neuropathy correlated with imbalanced Foxp3/IL-17 in bone marrow microenvironment of patients with acute myeloid leukemia

Chen Chen _, Yan Liu, Mingqiang Hua, Xiaomei Li, Chunyan Ji and Daoxin Ma

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Oncotarget. 2016; 7:24455-24465. https://doi.org/10.18632/oncotarget.8227

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Chen Chen1,2, Yan Liu2, Mingqiang Hua1, Xiaomei Li2, Chunyan Ji1, Daoxin Ma1

1Department of Hematology, Qilu Hospital, Shandong University, Jinan, China

2Taian City Central Hospital, Taian, China

Correspondence to:

Daoxin Ma, e-mail: daoxinma@sdu.edu.cn

Keywords: neuropathy, nerve-related molecules, T helper-related molecules, acute myeloid leukemia

Received: November 17, 2015    Accepted: March 04, 2016    Published: March 21, 2016


Bone marrow (BM) neural tissues are important components of bone marrow microenvironment and play important roles in normal hematopoiesis. Neuropathy of BM can cause immunological alteration in hematopoietic microenvironment. It also can induce the impairment of normal hematopoiesis and promote the development of hematologic diseases. In the present study, we determined the expression levels and clinical significances of nerve-related molecules [nestin, tyrosine hydroxylase (TH), Glial Fibrillary Acidic protein (GFAP) and S100B] and T helper-related molecules (IL-17, Foxp3) in BM of AML patients and controls by immunohistochemical analysis and RT-PCR. Our results showed that the positive rates and expression levels of nestin, TH, GFAP and IL-17 were significantly decreased while Foxp3 and the ratio of Foxp3/IL-17 were statistically elevated in BM of AML patients. We found that there were significantly positive correlations between nestin with TH and IL-17 in BM of AML patients. We also observed significantly negative correlations between nestin with TH and Foxp3/IL-17 ratio. Moreover, the expression of nestin was positively correlated with the overall survival of AML patients. Our study suggests that neuropathy together with imbalanced T helper immunology in bone marrow might play important roles in AML.

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