Open AccessCD4+CD25+ T Cells in primary malignant hypertension related kidney injury
Author(s) -
Hongdong Huang,
Yang Luo,
Yumei Liang,
Xi-Dai Long,
Youming Peng,
Zhihua Liu,
Xiaobin Wen,
Jia Meng,
Rong Tian,
Chengli Bai,
Li Cui,
Fuliang He,
Qiushi Lin,
Xueyan Wang,
Xiaoqun Dong
Publication year - 2016
Publication title -
scientific reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.24
H-Index - 213
ISSN - 2045-2322
DOI - 10.1038/srep27659
Subject(s) - il 2 receptor , kidney , pathogenesis , medicine , uric acid , acute kidney injury , flow cytometry , endocrinology , renal function , proteinuria , immunology , pathology , t cell , immune system
CD4 + CD25 + T cells are critical for maintenance of immunologic self-tolerance. We measured the number of CD4 + CD25 + cells in the patients with primary malignant hypertension related kidney injury, to explore the molecular pathogenesis of this disease. We selected 30 patients with primary malignant hypertension related kidney injury and 30 healthy volunteers. Information on clinical characteristics and laboratory tests was obtained from each subject. The number of CD4 + CD25 + cells and glomerular injury were assessed by flow cytometry and histopathology, respectively. Both serum IL-2, IL-4, and IL-6 and endothelial cell markers were analyzed by ELISA. ADAMTS13 antibody was detected by Western blotting. CD4 + CD25 + cells were significantly reduced in patients with primary malignant hypertension related kidney injury compared to controls ( P < 0.05). The number of CD4 + CD25 + cells was negatively related to blood urea nitrogen, serum uric acid, proteinuria, and supernatant IL-4; whereas positively associated with estimated glomerular filtration rate in patients. Gradually decreasing CD4 + CD25 + cells were also found as increasing renal injury. Additionally, patients exhibited increasing supernatant IL-4, serum IL-2 and IL-6, endothelial cell markers, and anti-ADAMTS13 antibody compared with controls (all P < 0.05). CD4 + CD25 + cells may play a key role in the pathogenesis of primary malignant hypertension related kidney injury.