1294 Proteomic profiling of CCCA reveals unique inflammatory and metabolic protein signature

Previous microarray data from CCCA patients have indicated profibrotic tendencies and dysregulated lipid pathways as characteristics of disease. Proteomic profiling was performed to better understand relevant disease pathways. Tissue samples were collected both affected vertex scalp unaffected occipital in five with CCCA. Differential protein expression defined >25% fold change p <.05. Of 5,444 proteins identified, 148 met criteria for differential expression. Among 51 upregulated expressed lesional CCCA, common included adaptive immune response (p <.001) immunoglobulin production <.001). Cholesterol biosynthesis the most pathway among 97 downregulated proteins, which downregulation FACR2 = 0.018) particularly notable. Our characterize a condition involving inflammatory metabolic changes that may contribute fibrosis. In comparison other cicatricial alopecias an established T cell response, deposition suggests B predominance. cells been implicated across range fibrotic pathologies vasculature, liver, lungs, skin. Preferentially cell-mediated fibrosis also involved dysfunction. Interestingly, has shown respond off-label use topical metformin, inhibits multiple lipogenic mechanisms including cholesterol biosynthesis. The complex relationship between metabolism tissue previously well demonstrated mouse models. Gene deletion FAR2, encodes FACR2, is associated scarring alopecia phenotype model, addition being extensive reduction skin surface lipids. This study identified warrant further investigation into biomarkers treatment targets