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CD4 + T Cells Have a Permissive Effect on Enriched Environment-Induced Hippocampus Synaptic Plasticity

Abstract : Living in an enriched environment (EE) benefits health by acting synergistically on various biological systems including the immune and the central nervous systems. The dialog between the brain and the immune cells has recently gained interest and is thought to play a pivotal role in beneficial effects of EE. Recent studies show that T lymphocytes have an important role in hippocampal plasticity, learning, and memory, although the precise mechanisms by which they act on the brain remain elusive. Using a mouse model of EE, we show here that CD4 + T cells are essential for spinogenesis and glutamatergic synaptic function in the CA of the hippocampus. However, CD4 + lymphocytes do not influence EE-induced neurogenesis in the DG of the hippocampus, by contrast to what we previously demonstrated for CD8 + T cells. Importantly, CD4 + T cells located in the choroid plexus have a specific transcriptomic signature as a function of the living environment. Our study highlights the contribution of CD4 + T cells in the brain plasticity and function. HIGHLIGHTS-CD4 + T cells play a major role in brain synaptic plasticity changes induced by an enriched environment in mice, as revealed by measurements of the CA hippocampus spinogenesis and glutamatergic synaptic function.-CD4 + T cells do not affect EE-induced neurogenesis in the dentate gyrus (DG) of the hippocampus, by contrast to CD8 + T cells as previously showed.-Brain CD4 + T cells sorted from dissected choroid plexus display a transcriptomic signature specific of the enriched environment as compared to standard environment as revealed by RNAseq.
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Submitted on : Tuesday, January 14, 2020 - 10:49:18 AM
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Zarif 2018 Frontiers in Sunapt...
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Evandro Moisés, Shaoyu Ge, Hadi Zarif, Salma Hosseiny, Agnes Paquet, et al.. CD4 + T Cells Have a Permissive Effect on Enriched Environment-Induced Hippocampus Synaptic Plasticity. Frontiers in Synaptic Neuroscience, Frontiers Media, 2018, 10 (14), ⟨10.3389/fnsyn.2018.00014⟩. ⟨inserm-02438295⟩



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