γδ17T Cells Hinder Mandibular Bone Defect Healing

mice, later inflammatory responses were diminished, resulting in accelerated repair. These findings suggest that IL-17-producing γδT cells (γδ17T cells) delay mandibular fracture repair by inhibiting inflammation resolution, thus prolonging the reparative phase. Targeting γδ17T cells or IL-17 may thus represent therapeutic strategies to enhance bone regeneration, particularly in challenging clinical settings involving mandibular fractures.