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

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

PROVIDER: PRJNA873941 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21210149_1.fastq.gz	Fastqsanger.gz
	SRR21210149_2.fastq.gz	Fastqsanger.gz
	SRR21210150_1.fastq.gz	Fastqsanger.gz
	SRR21210150_2.fastq.gz	Fastqsanger.gz

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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.

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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.

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

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whole brains from nicotinic acetylcholine receptor subunit mutant mice and littermate controls

Project description:Studies using mice with beta4 nicotinic acetylcholine receptor (nAChR) subunit deficiency (beta4-/- mice) helped reveal the roles of this subunit in bradycardiac response to vagal stimulation, nicotine-induced seizure activity and anxiety. In order to identify genes that might be related to beta4-containing nAChRs activity, we compared the mRNA expression profiles of brains from beta4-/- and wild-type mice using Affymetrix U74Avr2 microarray. Keywords: knockout mice, nicotinic acetylcholine receptor

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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

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

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

Project description: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.

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Project description:Major depressive disorder is one of the most common mental health conditions. Meningeal lymphatics are essential for drainage of molecules in the cerebrospinal fluid to the peripheral immune system. Their potential role in depression-like behaviour has not been investigated. Here, we show in mice, sub-chronic variable stress as a model of depression-like behaviour impairs meningeal lymphatics in females but not in males. Manipulations of meningeal lymphatics regulate the sex difference in the susceptibility to stress-induced depression- and anxiety-like behaviors in mice, as well as alterations of the medial prefrontal cortex and the ventral tegmental area, brain regions critical for emotional regulation. Together, our findings suggest meningeal lymphatic impairment contributes to susceptibility to stress in mice, and that restoration of the meningeal lymphatics might have potential for modulation of depression-like behaviour.

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

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