Interleukin-17 inhibits Adult Hippocampal Neurogenesis

被引:70
作者
Liu, Qiang [1 ,2 ]
Xin, Wei [1 ]
He, Ping [3 ]
Turner, Dharshaun [1 ]
Yin, Junxiang [1 ]
Gan, Yan [1 ]
Shi, Fu-Dong [1 ,2 ]
Wu, Jie [1 ,4 ]
机构
[1] St Josephs Hosp, Barrow Neurol Inst, Div Neurol, Phoenix, AZ 85013 USA
[2] Tianjin Med Univ, Gen Hosp, Tianjin Neurol Inst, Dept Neurol, Tianjin 300052, Peoples R China
[3] Arizona State Univ, Dept Chem Engn, Tempe, AZ USA
[4] Shantou Univ, Coll Med, Dept Physiol, Shantou, Guangdong, Peoples R China
基金
美国国家卫生研究院; 美国国家科学基金会;
关键词
NATURAL-KILLER-CELLS; NEURAL STEM-CELLS; INDUCED DEGENERATION; INDUCED DEPRESSION; T-CELLS; BRAIN; IL-17; NEURONS; RECEPTOR; EXCITABILITY;
D O I
10.1038/srep07554
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Interleukin 17(A) (IL-17) is a potent pro-inflammatory cytokine that acts as a central regulator of inflammatory response within the brain, but its physiological roles under non-inflammatory conditions remain elusive. Here we report that endogenous IL-17 ablates neurogenesis in the adult dentate gyrus (DG) of hippocampus. Genetic deletion of IL-17 increased the number of adult-born neurons in the DG. Further, we found that IL-17 deletion altered cytokine network, facilitated basal excitatory synaptic transmission, enhanced intrinsic neuronal excitability, and increased expression of proneuronal genes in neuronal progenitor cells (NPCs). Our findings suggest a profound role of IL-17 in the negative regulation of adult hippocampal neurogenesis under physiology conditions.
引用
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页数:8
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共 52 条
[51]   Distinct morphological stages of dentate granule neuron maturation in the adult mouse hippocampus [J].
Zhao, CM ;
Teng, EM ;
Summers, RG ;
Ming, GL ;
Gage, FH .
JOURNAL OF NEUROSCIENCE, 2006, 26 (01) :3-11
[52]   IL-17 induces apoptosis of vascular endothelial cells - A potential mechanism for human acute coronary syndrome [J].
Zhu, Faliang ;
Wang, Qun ;
Guo, Chun ;
Wang, Xiaoyan ;
Cao, Xuelei ;
Shi, Yongyu ;
Gao, Fei ;
Ma, Chunhong ;
Zhang, Lining .
CLINICAL IMMUNOLOGY, 2011, 141 (02) :152-160