Immunity to the microbiota promotes sensory neurons regeneration via IL-17A
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA809033 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18091051.fastq.gz | Fastqsanger.gz | |||
| SRR18091052.fastq.gz | Fastqsanger.gz | |||
| SRR18091053.fastq.gz | Fastqsanger.gz | |||
| SRR18091054.fastq.gz | Fastqsanger.gz | |||
| SRR18091055.fastq.gz | Fastqsanger.gz |
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Project description:Tissue physiology and responses to injury can be controlled by the cross-talk between all physiological systems including the nervous and immune system. How the microbiota influences this dialogue remains unclear. Here, we show that adaptive responses to the microbiota directly promote sensory neuron regeneration. At homeostasis, commensal-specific Th17 co-localize with sensory neurons within the dermis and display a transcriptional profile associated with tissue and nerve repair. Following injury, commensal-specific Th17 cells promote axon growth and local nerve regeneration. Mechanistically, our data support the idea that IL17-A produced by commensal-specific T cells directly signal sensory neurons via IL17RA, the transcription of which is specifically upregulated in injured neurons. Collectively our work reveals that microbiota-specific T cells can bridge biological systems by directly promoting neuronal repair and identify IL17-A as a major determinant of this fundamental process.
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