Bikram Dasgupta, Yuval Rinkevich
Fibroblasts are central architects of skin structure and repair, and their interactions with immune cells are essential for maintaining a normal healing trajectory. In this chapter, we discuss how fibroblasts arise from distinct developmental lineages with high regenerative potential, how they diversify across dermal layers in adulthood, and how these context-specific states shape wound outcomes. We outline the synchronized communication between fibroblast subsets, neutrophils, and macrophages driving controlled inflammation, organized matrix remodeling, and effective tissue restoration in acute injury. We contrast this with chronic wounds and fibro-proliferative disorders, where fibroblast-immune communication is altered, leading to persistent inflammation, excessive matrix deposition, or stalled repair. Together, these insights underscore fibroblast-immune crosstalk in regulating, maintaining, and subverting wound healing.