There is a large and growing clinical need for improved wound therapies. Skin wound healing involves the orchestrated communication and activities of macrophages with other wound effectors. Wound macrophages and fibroblasts respond dynamically to changes in their local physical and biochemical environment, presenting a target for engineered biomaterials to modulate cell-cell interaction in the wound bed. This dissertation examines the reciprocal signaling between macrophages and fibroblasts, and the potential of biophysical properties of engineered hydrogels to modulate this interaction to improve wound healing. Soft gelatin methacrylate (gelMA) hydrogel was shown to reduce scar size in small, full-thickness murine skin wounds, compared to stiff gelMA and no-treatment, additionally promoting a pro-healing macrophage phenotype in vitro and in vivo. Single-cell RNA sequencing of wound tissue treated with soft or stiff gelMA or no material at post wound day 5 revealed heterogeneous macrophage and fibroblast populations, with distinct shifts and differential gene expression in response to material stiffness. Cell-based wound closure assays in 2D and 3D were used to further parse these interactions, showing that juxtacrine co-culture of murine bone marrow derived macrophages with NIH 3T3 fibroblasts significantly enhanced fibroblast closure of 2D and 3D wounds. Coculture also altered macrophage activation in a contact-dependent manner, when compared to culture of ether cell type alone. Finally, broad inhibition of gap junctions with palmitoleic acid abrogated fibroblast enhanced macrophage IL-10 secretion and coculture enhanced calcium activity, suggesting that cell-cell contact through gap junctions may, in part, mediate macrophage-fibroblast communication. This work demonstrates a critical role for direct macrophage-fibroblast interactions in the cellular coordination of wound healing, and reveals the potential for targeting biophysical immunomodulation in the development of wound healing therapeutics.