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Meningeal gd T cells regulate anxiety like behaviors via Il17a signaling on Neurons

ABSTRACT: By characterizing the meningeal compartment of naive mice, here we explored a unique population of tissue-resident gd T cells, which we found to be the major source of IL-17A in the steady state meninges. gd T cells rapidly harbor meninges at perinatal stages and actively make IL-17A. Their IL-17A production was TCR-dependent but it occurred independent of commensal microbiota. The absence of meningeal gd T cells was related with risk-taking behavior in mice, which was dependent on the IL-17A signaling directly in the prefrontal cortex neurons. Our results demonstrate that tissue-resident meningeal gd T cell-derived IL-17A may represent an evolutionary bridge between anti-pathogen response and avoidance behavioral traits in vertebrates.

ORGANISM(S): Mus musculus

PROVIDER: GSE132047 | GEO | 2020/07/24

REPOSITORIES: GEO

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Meningeal gd T cells regulate anxiety like behaviors via Il17a signaling on Neurons (PFC neurons)

Project description:Interleukin 17a (IL-17a) is a cytokine that has been highly conserved during evolution of the vertebrate immune system and widely studied in contexts of infection and autoimmunity. Recent studies in mouse models of maternal immune activation suggest that IL-17a is also linked to behavioral changes reminiscent of those seen under pathological conditions such as autism spectrum disorders (ASD)1 and in aggregation behavior in Caenorhabditis elegans2, raising the intriguing possibility that this cytokine might have evolved for the homeostatic regulation of neuronal activity. Here, by in-depth cellular and molecular characterization of a unique population of meningeal-resident gd17 T cells, we characterized the nearest central nervous system (CNS)-associated source of IL-17a under homeostasis. Meningeal gd T cell-derived IL-17a was associated with anxiety-like behaviors in mice, which partially depended on T-cell receptor engagement and commensal microbiota. IL-17a receptor was highly expressed in glutamatergic neurons under steady state and its genetic deletion decreased anxiety-like behavior in mice by shaping the transcriptional landscape and synaptic transmission of neurons in the medial prefrontal cortex (mPFC). From an evolutionary perspective, these findings suggest that IL-17a production by tissue-resident meningeal gd17 T cells may represent an evolutionary bridge between conserved anti-pathogen molecules and avoidance/survival behavioral traits in vertebrates.

2020-07-24 | GSE147261 | GEO

Meningeal gd T cells regulate anxiety like behaviors via Il17a signaling on Neurons (DG neurons)

2020-07-24 | GSE147260 | GEO

Meningeal gd T cells regulate anxiety like behaviors via Il17a signaling on Neurons

Project description:Meningeal gd T cells regulate anxiety like behaviors via Il17a signaling on Neurons

| PRJNA613628 | ENA

Meningeal gd T cells regulate anxiety like behaviors via Il17a signaling on Neurons

Project description:Meningeal gd T cells regulate anxiety like behaviors via Il17a signaling on Neurons

| PRJNA545716 | ENA

Meningeal natural killer cells and innate lymphoid cells 1 tune anxiety and memory via interferon-γ and acetylcholine

Project description:The mechanisms of communication between the brain and the neighboring meningeal immune cells are still unclear. Here we characterized the resident group 1 innate lymphoid cells in the meninges of adult mice, and identified ILC1/NK cell-derived interferon- and acetylcholine as mediators involved in the modulation of brain circuitries underlying anxiety-like behavior and memory. This discloses a new meningeal-to-brain communication mechanism that modulates brain functions under physiological conditions.

2023-05-05 | GSE212089 | GEO

Meningeal gd T cells regulate anxiety like behaviors via Il17a signaling on Neurons (DG neurons)

Project description:Meningeal gd T cells regulate anxiety like behaviors via Il17a signaling on Neurons (DG neurons)

| PRJNA613633 | ENA

Meningeal gd T cells regulate anxiety like behaviors via Il17a signaling on Neurons (PFC neurons)

Project description:Meningeal gd T cells regulate anxiety like behaviors via Il17a signaling on Neurons (PFC neurons)

| PRJNA613632 | ENA

Characterization of meningeal type 2 innate lymphocytes and their response to CNS injury

Project description:The meningeal space is occupied by a diverse repertoire of innate and adaptive immune cells. CNS injury elicits a rapid immune response that affects neuronal survival and recovery, but the role of meningeal inflammation in CNS injury remains poorly understood. Here we describe group 2 innate lymphoid cells (ILC2s) as a novel cell type resident in the healthy meninges that is activated following CNS injury. ILC2s are present throughout the naïve mouse meninges, though are concentrated around the dural sinuses, and have a unique transcriptional profile relative to lung ILC2s. After spinal cord injury, meningeal ILC2s are activated in an IL-33 dependent manner, producing type 2 cytokines. Using RNAseq, we characterized the gene programs that underlie the ILC2 activation state. Finally, addition of wild type lung-derived ILC2s into the meningeal space of IL-33R-/- animals improves recovery following spinal cord injury. These data characterize ILC2s as a novel meningeal cell type that responds to and functionally affects outcome after spinal cord injury, and could lead to new therapeutic insights for CNS injury or other neuroinflammatory conditions.

2016-12-13 | GSE90908 | GEO

Meningeal γδ T cells producing IL-17 control synaptic plasticity and cognitive behaviour

Project description:The conventional notion of “immune privilege” of the brain has been revised to accommodate its infiltration, at steady state, by immune cells that participate in normal neurophysiology (Louveau, Trends Immunol 2015; Kipnis science 2016; Filiano, Nat Rev Neurosciences 2017). Surprisingly, such neuroimmune functions have been linked to “pro-inflammatory” cytokines like IL-4 or IFN-α, shown to control behavioural and social cognition (Derecki, JEM 2010; Filiano, Nature 2016). Here we identify a pro-cognitive role for IL-17 in short-term memory that derives from a previously unknown meningeal-resident γδ T cell subset. This was mostly composed of foetal thymic-derived Vγ6+ T cells, found in the meninges at birth and persisting throughout life, where they were strikingly polarized towards IL-17 production. In fact, γδ T cells were the overwhelming source of meningeal IL-17, whereas IFN-γ was mostly provided by T cells. To assess whether the constitutive production of IL-17 by γδ T cells influenced the cognitive performance of mice, we tested TCRδ-/-, IL-17-/- and respective WT littermate control mice in classical learning paradigms. We observed that mice deficient either for γδ T cells or IL-17 displayed impaired short-term memory in the Y maze paradigm, while retaining normal long-term spatial memory in the Morris water maze. A detailed proteomics analysis of the hippocampus provided mechanistic insight into reduced plasticity of the glutamatergic synapses in the absence of IL-17, which associated with impaired Long Term Potentiation (LTP). Conversely, IL-17 enhanced glial cell production of Brain Derived Neurotropic Factor (BDNF), whose exogenous provision rescued the LTP defect of IL-17-/- animals. Altogether, our data demonstrate that foetal-derived γδ T cells populate the brain meninges where they regulate synaptic plasticity and short-term memory through a non-inflammatory IL-17-dependent mechanism.

2019-10-16 | PXD007574 | Pride

Infection drives long-term meningeal engraftment by inflammatory monocytes that impair central nervous system immunity [II]

Project description:Tissue-resident macrophages have an embryonic origin, but are replenished under steady state conditions in some tissues by blood monocytes that can adopt genotypic and phenotypic features of the residents. However, little is known about the residency and functional properties of infiltrating macrophages after an inflammatory challenge. The meninges of the central nervous system (CNS) are populated by a dense network of specialized macrophages that act as resident immune sentinels. Here we show that following lymphocytic choriomeningitis virus infection resident meningeal macrophages become activated by innate inflammatory cytokines, acquire viral antigen, and interact directly with infiltrating cytotoxic T lymphocytes (CTL), which leads to their depletion. Concurrently, the meninges are heavily infiltrated by peripherally-derived inflammatory monocytes that engraft the meningeal niche and remain in situ for months after viral clearance. This engraftment leads to phenotypic and functional changes in the pool of resident meningeal macrophages that depends in part on IFNγ signaling. These changes include loss of bacterial and immunoregulatory sensors that impede subsequent CNS immune reactions. Collectively, these data indicate that peripheral monocytes can engraft the meninges after an inflammatory challenge, imprinting the compartment with long-term defects in immune function.

2019-03-06 | GSE108647 | GEO

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