Journal
CELL
Volume 179, Issue 4, Pages 864-+Publisher
CELL PRESS
DOI: 10.1016/j.cell.2019.10.001
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Funding
- National Key R&D Program of China [2018YFA0800503, 2018YFD0500100]
- Excellent Young Scientist Fund of NSFC [31822017]
- Zhejiang Provincial Natural Science Foundation of China [LR19C080001]
- Strategic Priority Research Program of the Chinese Academy of Science [XDA16010302]
- National Natural Science Foundation of China [81572651, 81771675, 81622013, 81700913]
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Physical or mental stress leads to neuroplasticity in the brain and increases the risk of depression and anxiety. Stress exposure causes the dysfunction of peripheral T lymphocytes. However, the pathological role and underlying regulatory mechanism of peripheral T lymphocytes in mood disorders have not been well established. Here, we show that the lack of CD4(+) T cells protects mice from stress-induced anxiety-like behavior. Physical stress-induced leukotriene B4 triggers severe mitochondrial fission in CD4(+) T cells, which further leads to a variety of behavioral abnormalities including anxiety, depression, and social disorders. Metabolomic profiles and single-cell transcriptome reveal that CD4(+) T cell-derived xanthine acts on oligodendrocytes in the left amygdala via adenosine receptor A1. Mitochondrial fission promotes the de novo synthesis of purine via interferon regulatory factor 1 accumulation in CD4(+) T cells. Our study implicates a critical link between a purine metabolic disorder in CD4(+) T cells and stress-driven anxiety-like behavior.
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