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MrgprD-expressing neurons maintain cutaneous mast cell homeostasis

ABSTRACT: MrgprD-expressing neurons maintain cutaneous mast cell homeostasis

PROVIDER: PRJNA600963 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10879550_1.fastq.gz	Fastqsanger.gz
	SRR10879550_2.fastq.gz	Fastqsanger.gz
	SRR10879551_1.fastq.gz	Fastqsanger.gz
	SRR10879551_2.fastq.gz	Fastqsanger.gz
	SRR10879552_1.fastq.gz	Fastqsanger.gz

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Nonpeptidergic MrgprD-expressing neurons maintain cutaneous homeostasis via glutamate-mediated mast cell suppression

Project description:Cutaneous mast cells (MC) mediate numerous skin inflammatory processes and have anatomical and functional associations with sensory afferent neurons. We found that Langerhans cell (LC)-deficient mice have reduced numbers of MrgprD-expressing epidermal nerve endings and manifest enhanced irritant dermatitis due to exaggerated MC degranulation. Ablation of LC or MrgprD-expressing neurons increased expression of a MC gene module including the activating receptor, Mrgprb2, resulting in increased MC degranulation and cutaneous inflammation in multiple models. β-alanine agonism of MrgprD-expressing neurons reduced expression of MC module genes and suppressed MC responses. MrgprD-expressing neurons released glutamate which was increased by MrgprD agonism and decreased in LC-deficient mice. Inhibiting glutamate release or glutamate receptor binding yielded hyperresponsive MC and a genomic state similar to that in mice lacking MrgprD-expressing neurons. These data demonstrate that MrgprD-expressing neurons suppress MC hyperresponsiveness and skin inflammation via glutamate release thereby revealing an unexpected neuro-immune mechanism maintaining cutaneous immune homeostasis.

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