<p>Wound healing is a multifaceted and dynamic sequence of tissue repair and regeneration processes involving interrelated stages: inflammation, regeneration, and remodeling. Throughout these processes, macrophages change their phenotypes and interact with cells and extracellular components to facilitate healing. In particular, macrophages expressing the surface marker CD206 associate with inflammation resolution and tissue repair. However, how CD206⁺ macrophages contribute to these processes is insufficiently understood. Here, using a mouse model of CD206⁺ macrophage depletion and single-cell transcriptomics, we report that selective depletion of CD206⁺ macrophages results in modest but significant delays in wound healing, prolongs inflammation, and significantly reduces the number of <i>Gpnmb</i>^hi fibroblasts in injured skin. Single-cell data suggest that CD206⁺ macrophages communicate with <i>Gpnmb</i>^hi fibroblasts via multiple pathways. Notably, topical administration of PDGF-AA to wounds of CD206⁺ macrophage-depleted mice restores healing processes, identifying PDGF-A signaling from CD206⁺ macrophages to PDGFRA on fibroblasts as an important mechanism promoting wound healing. Collectively, these data demonstrate that CD206⁺ macrophages communicate with <i>Gpnmb</i>^hi fibroblasts to activate their proliferation and extracellular matrix deposition in wound healing.</p>