Tissue repair processes maintain proper organ function following mechanical or infection-related damage. In addition to antibacterial properties, mucosal associated invariant T (MAIT) cells express a tissue repair transcriptomic program and promote skin wound healing when expanded. Herein, we use a human-like mouse model of full-thickness skin excision to assess the underlying mechanisms of MAIT cell tissue repair function. Single-cell RNA sequencing analysis suggested that skin MAIT cells already express a repair program at steady state. Following skin excision, MAIT cells promoted keratinocyte proliferation, thereby accelerating healing. Using skin grafts, parabiosis, and adoptive transfer experiments, we show that MAIT cells migrated into the wound in a T cell receptor (TCR)-independent but CXCR6 chemokine receptor-dependent manner. Amphiregulin secreted by MAIT cells following excision promoted wound healing. Expression of the repair function was probably independent of sustained TCR stimulation. Overall, our study provides mechanistic insights into MAIT cell wound healing function in the skin. [Display omitted] • MAIT cells accelerate wound closure in a human-like skin injury model • MAIT cells migrate into the inflamed skin via CXCR6/CXCL16 and independently of MR1 • MAIT cell pro-repair function is independent of sustained TCR signaling • Amphiregulin production by MAIT cells accelerates wound closure MAIT cells have tissue repair properties, but the underlying mechanisms are unclear. du Halgouet et al. demonstrate that MAIT cells accelerate wound closure by increasing epithelial proliferation. MAIT cells are recruited into the injured skin in a CXCL16/CXCR6-dependent MR1-independent manner, and their pro-repair effect is related to amphiregulin production. [ABSTRACT FROM AUTHOR]