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An extraordinary recent study by Enamorado et al. 1 has, for the first time, demonstrated that immunity to the microbiota enhances repair of sensory nerves and epithelial tissues within the skin. Colonization of the skin by Staphylococcus aureus (SA) generated commensal-specific interleukin (IL)-17–producing CD4+ T helper 17 (Th17) cells that accelerated repair of cutaneous nerve fibers and restored normal sensory thresholds. Remarkably, this “type 17 immunity” evoked minimal inflammation or pain and had no detrimental effect on host immunity to further infections by different SA strains.

The study advances our knowledge on the multiple bidirectional interactions between peripheral sensory nerve fibers and resident cutaneous immune cells that are only recently being characterized and interrogated using contemporary high-dimensional analyses. These diverse interactions play numerous roles in host defense, tissue repair and pain transmission. Host defense is an area in which there are many exciting