Evidence for Resident Memory T Cells and Necroptosis as Drivers of Fibrosis in Eosinophilic Fasciitis and Morphea

This study investigates the pathogenesis of eosinophilic fasciitis (EF) and morphea, focusing on the role of resident memory T cells (TRM) and necroptosis in driving fibrosis. By analyzing skin biopsies from patients with established fibrosis and comparing them to healthy skin, researchers found significant upregulation of cytotoxic injury signatures and T cell activation genes, despite a lack of inflammatory appearance. The study highlights the potential involvement of TRM in chronic fibrosis and identifies necroptosis as a key process, with increased expression of necroptosis effector RIPK3 in EF and morphea. Immunostaining showed increased T cell-associated apoptotic and necroptotic endothelial cells, suggesting T cell-driven vascular injury. The findings propose that targeting TRM or necroptosis could be a novel therapeutic approach for treating cutaneous fibrosis.