Immunity to the microbiota promotes sensory neuron regeneration

Tissue immunity and responses to injury depend on the coordinated action and communication among phys-iological systems. Here, we show that, upon injury, adaptive responses to the microbiota directly promote sensory neuron regeneration. At homeostasis, tissue-resident commensal-specific T cells colocalize with sensory nerve fibers within the dermis, express a transcriptional program associated with neuronal interac-tion and repair, and promote axon growth and local nerve regeneration following injury. Mechanistically, our data reveal that the cytokine interleukin-17A (IL-17A) released by commensal-specific Th17 cells upon injury directly signals to sensory neurons via IL-17 receptor A, the transcription of which is specifically upregulated in injured neurons. Collectively, our work reveals that in the context of tissue damage, preemptive immunity to the microbiota can rapidly bridge biological systems by directly promoting neuronal repair, while also iden-tifying IL-17A as a major determinant of this fundamental process.

Automated summary

Tissue immunity and responses to injury rely on coordinated action and communication among physiological systems. The study demonstrates that adaptive responses to the microbiota can directly promote sensory neuron regeneration after injury. The researchers found that commensal-specific T cells in the skin tissue express neuronal interaction and repair genes, promoting axon growth and local nerve regeneration. The cytokine IL-17A released by these T cells signals to sensory neurons, indicating its importance in the process.