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

Zarif, Hadi; Hosseiny, Salma; Paquet, Agnès; Lebrigand, Kévin; Arguel, Marie-Jeanne; Cazareth, Julie; Lazzari, Anne; Heurteaux, Catherine; Glaichenhaus, Nicolas; Chabry, Joëlle; Guyon, Alice; Petit-Paitel, Agnès

doi:10.3389/fnsyn.2018.00014

Cited by 14 publications

(11 citation statements)

References 28 publications

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“…Recent findings suggest that dysregulated infiltration of the brain parenchyma by peripheral immune cells, such as T cells and antigen-presenting cells of the monocyte-macrophage lineage, may be involved in the etiology of SZ 11 . Peripheral CD4 + T cells are thought to be involved in CNS surveillance 12 , adult hippocampal neurogenesis, and synaptic plasticity, thereby influencing learning and social behavior, potentially reflecting that these T cells are passing the blood-brain barrier (BBB) [13][14][15][16][17][18][19] . Consistent with this hypothesis, several human genetic studies have identified polymorphisms in or near CAM genes that are associated with developmental neuropsychiatric disorders such as autism spectrum disorders and SZ 8,20 .…”

Section: Introductionmentioning

confidence: 99%

Reduced levels of circulating adhesion molecules in adolescents with early-onset psychosis

et al. 2020

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It is suggested that neurodevelopmental abnormalities are involved in the disease mechanisms of psychotic disorders. Although cellular adhesion molecules (CAMs) participate in neurodevelopment, modulate blood-brain barrier permeability, and facilitate leukocyte migration, findings concerning their systemic levels in adults with psychosis are inconsistent. We examined plasma levels and mRNA expression in peripheral blood mononuclear cells (PBMCs) of selected CAMs in adolescents with early-onset psychosis (EOP) aged 12-18 years (n = 37) and age-matched healthy controls (HC) (n = 68). EOP patients exhibited significantly lower circulating levels of soluble platelet selectin (~−22%) and soluble vascular cell adhesion molecule-1 (~−14%) than HC. We found no significant associations with symptom severity. PSEL mRNA expression was increased in PBMCs of patients and significantly negatively correlated to duration of illness. These findings suggest a role for CAMs in the pathophysiology of psychotic disorders.

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Section: Introductionmentioning

confidence: 99%

Reduced levels of circulating adhesion molecules in adolescents with early-onset psychosis

et al. 2020

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“…In a previous study, we showed that CD4 + T cells play a major role in EE-induced changes of hippocampus synaptic plasticity [1]. A large proportion of T cells in the brain are located in the choroid plexus, a highly vascularized structure made of endothelial and epithelial cells that produces CSF from blood.…”

Section: Discussionmentioning

confidence: 99%

“…Eight days after the last antibody injection, the mice were sacrificed, spleens were harvested, and immune cells prepared to control for the absence of CD4 + T cells by using flow cytometry with the anti-CD3 and anti-CD4 antibodies. No depletion was observed in control Ab-injected mice spleen, while around 98% depletion was observed with the anti-CD4 antibody [1]. …”

Section: Methodsmentioning

confidence: 99%

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CD4<sup>+</sup> T Cells Affect the Thyroid Hormone Transport at the Choroid Plexus in Mice Raised in Enriched Environment

Zarif

Paquet

Lebrigand

et al. 2019

Neuroimmunomodulation

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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.

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“…The circulation of T-lymphocytes in the brain occurs physiologically, since the early development, and persists during adulthood, to guarantee synaptic plasticity [8,207,208]. For instance, both CD4+ and CD8+ T-cells are essential for spinogenesis and GLUT synaptic function in the hippocampus [209]. In addition, CD8+ T cells regulate the hippocampal volume by promoting neurogenesis [210].…”

Section: Autophagy and Proteasome Tune Synaptic Plasticity By Modumentioning

confidence: 99%

Cell Clearing Systems Bridging Neuro-Immunity and Synaptic Plasticity

Limanaqi

Biagioni

Busceti

et al. 2019

IJMS

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In recent years, functional interconnections emerged between synaptic transmission, inflammatory/immune mediators, and central nervous system (CNS) (patho)-physiology. Such interconnections rose up to a level that involves synaptic plasticity, both concerning its molecular mechanisms and the clinical outcomes related to its behavioral abnormalities. Within this context, synaptic plasticity, apart from being modulated by classic CNS molecules, is strongly affected by the immune system, and vice versa. This is not surprising, given the common molecular pathways that operate at the cross-road between the CNS and immune system. When searching for a common pathway bridging neuro-immune and synaptic dysregulations, the two major cell-clearing cell clearing systems, namely the ubiquitin proteasome system (UPS) and autophagy, take center stage. In fact, just like is happening for the turnover of key proteins involved in neurotransmitter release, antigen processing within both peripheral and CNS-resident antigen presenting cells is carried out by UPS and autophagy. Recent evidence unravelling the functional cross-talk between the cell-clearing pathways challenged the traditional concept of autophagy and UPS as independent systems. In fact, autophagy and UPS are simultaneously affected in a variety of CNS disorders where synaptic and inflammatory/immune alterations concur. In this review, we discuss the role of autophagy and UPS in bridging synaptic plasticity with neuro-immunity, while posing a special emphasis on their interactions, which may be key to defining the role of immunity in synaptic plasticity in health and disease.

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

Cited by 14 publications

References 28 publications

Reduced levels of circulating adhesion molecules in adolescents with early-onset psychosis

Reduced levels of circulating adhesion molecules in adolescents with early-onset psychosis

CD4<sup>+</sup> T Cells Affect the Thyroid Hormone Transport at the Choroid Plexus in Mice Raised in Enriched Environment

Cell Clearing Systems Bridging Neuro-Immunity and Synaptic Plasticity

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