BACKGROUND Others and we have shown that T cells have an important role in hippocampal synaptic plasticity, including neurogenesis in the dentate gyrus, spinogenesis, and glutamatergic synaptic function in the CA of the hippocampus. Hippocampus plasticity is particularly involved in the brain effects of the enriched environment (EE), and interestingly CD4+ and CD8+ T cells play essential and differential roles in these effects. However, the precise mechanisms by which they act on the brain remain elusive. OBJECTIVES We searched for a putative mechanism of action by which CD4+ T cells could influence brain plasticity and hypothesized that they could regulate protein transport at the level of the blood-CSF barrier in the choroid plexus. METHOD We compared mice housed in EE and deprived of CD4+ T cells using a depleting antibody with a control group injected with the control isotype. We analyzed in the hippocampus the gene expression profiles using the Agilent system, and the expression of target proteins in plasma, CSF, and the choroid plexus using ELISA. RESULTS We show that CD4+ T cells may influence EE-induced hippocampus plasticity via thyroid hormone signaling by regulating in the choroid plexus the expression of transthyretin, the major transporter of thyroxine (T4) to the brain parenchyma. CONCLUSIONS Our study highlights the contribution of close interactions between the immune and neuroendocrine systems in brain plasticity and function.

中文翻译：

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CD4 + T细胞影响在富集环境中饲养的小鼠的脉络丛中甲状腺激素转运。

背景其他人和我们已经表明，T细胞在海马突触可塑性中具有重要作用，包括齿状回中的神经发生，棘突发生和海马CA中的谷氨酸能突触功能。海马可塑性特别参与丰富环境（EE）的大脑效应，有趣的是CD4 +和CD8 + T细胞在这些效应中起着至关重要的作用。但是，它们作用于大脑的确切机制仍然难以捉摸。目的我们寻找一种假定的作用机制，通过该机制，CD4 + T细胞可以影响大脑的可塑性，并假设它们可以调节脉络丛中血液CSF屏障水平的蛋白质转运。方法我们比较了使用耗尽抗体的EE小鼠和被剥夺CD4 + T细胞的小鼠与注射了对照同种型的对照组。我们使用Agilent系统分析了海马中的基因表达谱，并使用ELISA分析了血浆，CSF和脉络丛中靶蛋白的表达。结果我们显示，CD4 + T细胞可能通过调节脉络丛中甲状腺素（T4）向脑实质的主要转运蛋白-甲状腺素的表达，通过甲状腺激素信号传导来影响EE诱导的海马可塑性。结论我们的研究强调了免疫系统和神经内分泌系统之间紧密相互作用对大脑可塑性和功能的贡献。ELISA检测靶蛋白在血浆，CSF和脉络丛中的表达。结果我们显示，CD4 + T细胞可能通过调节脉络丛中甲状腺素（T4）向脑实质的主要转运蛋白-甲状腺素的表达，通过甲状腺激素信号传导来影响EE诱导的海马可塑性。结论我们的研究强调了免疫系统和神经内分泌系统之间紧密相互作用对大脑可塑性和功能的贡献。ELISA检测靶蛋白在血浆，CSF和脉络丛中的表达。结果我们显示，CD4 + T细胞可能通过调节脉络丛中甲状腺素（T4）向脑实质的主要转运蛋白-甲状腺素的表达，通过甲状腺激素信号传导来影响EE诱导的海马可塑性。结论我们的研究强调了免疫系统和神经内分泌系统之间紧密相互作用对大脑可塑性和功能的贡献。