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Temporal kinetics of CD8 + CD28 + and CD8 + CD28 − T lymphocytes in the injured rat spinal cord
Author(s) -
Wu Yan,
Lin YuHong,
Shi LingLing,
Yao ZongFeng,
Xie XiuMei,
Jiang ZhengSong,
Tang Jie,
Hu JianGuo,
Lü HeZuo
Publication year - 2017
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.23993
Subject(s) - cytotoxic t cell , cd28 , cd8 , flow cytometry , microbiology and biotechnology , propidium iodide , spinal cord injury , chemistry , biology , medicine , immunology , pathology , apoptosis , spinal cord , immune system , in vitro , programmed cell death , biochemistry , neuroscience
This study aims to explore the temporal changes of cytotoxic CD8 + CD28 + and regulatory CD8 + CD28 − T‐cell subsets in the lesion microenvironment after spinal cord injury (SCI) in rats, by combination of immunohistochemistry (IHC) and flow cytometry (FCM). In the sham‐opened spinal cord, few CD8 + T cells were found. After SCI, the CD8 + T cells were detected at one day post‐injury (dpi), then markedly increased and were significantly higher at 3, 7, and 14 dpi compared with one dpi (p < 0.01), the highest being seven dpi. In CD8 + T cells, more than 90% were CD28 + , and there were only small part of CD28 − ( < 10%). After 14 days, the infiltrated CD8 + T cells were significantly decreased, and few could be found in good condition at 21 and 28 dpi. Annexin V and propidium iodide (PI) staining showed that the percentages of apoptotic/necrotic CD8 + cells at 14 dpi and 21 dpi were significantly higher than those of the other early time‐points (p < 0.01). These results indicate that CD8 + T cells could rapidly infiltrate into the injured spinal cords and survive two weeks, however, cytotoxic CD8 + T cells were dominant. Therefore, two weeks after injury might be the “time window” for treating SCI by prolonging survival times and increasing the fraction of CD8 + regulatory T‐cells. © 2016 Wiley Periodicals, Inc.