Systemic sclerosis, also known as scleroderma (SSc), remains one of the most dangerous autoimmune diseases because it scars multiple organs and has few effective treatments. Lung involvement, called SSc-associated interstitial lung disease, stands as a leading cause of death. This project investigates cadherin-11 (Cdh11), a molecule the research team recently identified as a key driver of skin and lung fibrosis, to determine how it controls the cells that form harmful scar tissue. The work explores how Cdh11 influences macrophages, alveolar epithelial cells, and fibroblasts, the major cell types that shape lung structure. Specialized transgenic mouse models enable the precise removal of Cdh11 from each cell type, revealing its specific role in disease progression. Transcriptomic analyses map the genetic pathways controlled by Cdh11 and identify related regulators, such as MafB, that may open new treatment options. Results from this effort aim to deliver two practical advances. First, a clearer understanding of the biological mechanisms that trigger lung fibrosis in systemic sclerosis is needed. Second, identification of new therapeutic targets, including the potential to use Cdh11 to guide nanocarrier-based treatments directly to diseased tissue.