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Expression of breast cancer resistance protein in peripheral T cell subsets from HIV-1-infected patients with antiretroviral therapy
Author(s) -
Jiu-Cong Zhang,
Zhi-Yun Deng,
Yong Wang,
Fang Xie,
Li Sun,
Fangxin Zhang
Publication year - 2014
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2014.2282
Subject(s) - cd8 , peripheral blood mononuclear cell , immunology , flow cytometry , oncogene , cancer , molecular medicine , medicine , breast cancer , t cell , cell cycle , biology , immune system , biochemistry , in vitro
The aim of the present study was to investigate the expression of breast cancer resistance protein (BCRP) in peripheral T cell subsets of human immunodeficiency virus 1 (HIV‑1)‑infected patients, and to analyze the association between the levels of BCRP expression and disease progression in HIV‑1 infection. Peripheral blood mononuclear cells (PBMCs) were obtained from HIV‑1‑infected patients (n=118), including 92 patients with antiretroviral therapy (ART) and 26 patients without a history of ART. Control samples from 30 healthy donors were also analyzed. The expression levels of BCRP in T cells were evaluated by flow cytometry. A high inter‑individual variability was observed in CD4+ and CD8+ T cells in the HIV‑1‑infected patients and healthy donors; however, the analyzed expression levels of BCRP were significantly higher in the HIV‑1‑infected group with ART than those in the group with no history of ART (P<0.01). Furthermore, the frequency of BCRP‑expressing T cells was inversely correlated with CD4+ and CD8+ T cell counts in HIV‑1‑infected patients with ART. The results suggested that BCRP expression varied among HIV‑1‑infected patients and healthy donors but was significantly higher in HIV‑1 patients undergoing ART. In conclusion, the present study suggested that overexpression of BCRP may be involved in disease progression of the HIV‑1 infection and may participate in drug resistance to ART, thus contributing to the failure of highly active ART in HIV‑1 therapeutics.

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