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Group 2 innate lymphoid cells promote inhibitory synapse development and social behavior

ABSTRACT: Group 2 innate lymphoid cells promote inhibitory synapse development and social behavior

PROVIDER: PRJNA989527 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25083629.fastq.gz	Fastqsanger.gz
	SRR25083630.fastq.gz	Fastqsanger.gz
	SRR25083631.fastq.gz	Fastqsanger.gz
	SRR25083632.fastq.gz	Fastqsanger.gz

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Group 2 innate lymphoid cells promote inhibitory synapse development and social behavior

Project description:The innate immune system plays essential roles in brain development, including the remodeling of neuronal synapses. Innate lymphocytes are the most recently discovered member of the innate immune arsenal, whose developmental expansion and activation make them potential mediators of brain-immune communication during synapse formation. Here we show that group 2 innate lymphoid cells (ILC2s) and their cytokine Interleukin-13 (IL-13) signal directly to inhibitory interneurons to increase inhibitory synapse density in the developing brain. ILC2s expanded and produced IL-13 in the developing brain meninges. Loss of ILC2s or IL-13 signaling to interneurons decreased inhibitory, but not excitatory, cortical synapses. Conversely, ILC2s and IL-13 were sufficient to increase inhibitory synapses. Loss of this signaling pathway led to selective impairments in social interaction. These data define a type 2 neuroimmune circuit in early life that shapes inhibitory synapse development and behavior.

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Project description:Group 2 innate lymphoid cells promote inhibitory synapse development and social behavior [snRNA-Seq]

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Group 2 innate lymphoid cells promote inhibitory synapse development and social behavior.

Project description:The innate immune system plays essential roles in brain synaptic development, and immune dysregulation is implicated in neurodevelopmental diseases. Here we show that a subset of innate lymphocytes (group 2 innate lymphoid cells, ILC2s) is required for cortical inhibitory synapse maturation and adult social behavior. ILC2s expanded in the developing meninges and produced a surge of their canonical cytokine Interleukin-13 (IL-13) between postnatal days 5-15. Loss of ILC2s decreased cortical inhibitory synapse numbers in the postnatal period where as ILC2 transplant was sufficient to increase inhibitory synapse numbers. Deletion of the IL-4/IL-13 receptor (Il4ra) from inhibitory neurons phenocopied the reduction inhibitory synapses. Both ILC2 deficient and neuronal Il4ra deficient animals had similar and selective impairments in adult social behavior. These data define a type 2 immune circuit in early life that shapes adult brain function.

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