Cutaneous lupus erythematosus (CLE) is a chronic inflammatory skin disease characterized by marked clinical and molecular heterogeneity. A central role in the pathogenesis is the activation of the type I interferon (IFN) signaling pathway, although the extent of this activation varies among patients as well as across different cell types and tissue compartments. Established therapies such as hydroxychloroquine or other immunosuppressants are not equally effective in all patients. As part of the Memorial Fellowship, this project will investigate the extent to which molecular signatures can contribute to the characterization of disease activity and treatment response. To this end, clinical data will be combined with expression analyses of skin samples, functional studies on primary cells, and longitudinal immunophenotyping of peripheral blood. The goal is to identify molecular endotypes that enable better risk stratification and personalized treatment decisions for CLE.