The immune system plays a critical role in the regeneration of the peripheral nervous system post-injury (1,2), though the role of T lymphocytes remains poorly understood. With recent evidence that IL-17A-producing T cells promote tissue homeostasis(3,4), we hypothesised that this cytokine could regulate the repair of peripheral nerve after traumatic injury. We show that γδ T cells are a major source of IL-17A (henceforth IL-17) in the injured nerve and that IL-17+ cells are present in the nerve throughout recovery. In animals without IL-17 expression, nerve electrophysiology shows increased spike numbers with higher energy, showing a critical role in impulse regulation. Mechanistically, lack of IL-17 is associated with increased growth-associated protein 43 (GAP-43) expression, a molecule expressed by both growing axons and Schwann cells (SC), but has no impact on axon-specific SCG-10, suggesting that IL-17 regulates SC physiology in this context.