Until now, functionally distinct subclasses of fibroblasts have proven difficult to define, characterize and study in health and disease. In contrast, the identification of leucocyte subsets with non-overlapping effector functions has provided a molecular framework for the development of targeted therapies that have demonstrated spectacular success in immune-mediated inflammatory diseases (IMIDs). Furthermore, it remains unknown whether fibroblast mediated inflammation, its resolution; tissue damage and repair are always coupled, reflecting cellular plasticity residing within single fibroblast populations or instead, are uncoupled and mediated by different subsets of fibroblasts. In this lecture I will explain the interrelationships between fibroblast subsets and observe how selective deletion of these subsets or changes in their biology alter the balance between persistent inflammation, tissue damage and fibrosis during the development of pathology .