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Millions of people suffer from psoriasis, a chronic, autoimmune disorder that causes scaly patches on the skin and often precedes psoriatic arthritis. While no cure exists, treatments range from topical creams to injected medications that block inflammation. To improve treatment options, scientists need to better understand the dysregulation of the immune system that leads to these lesions.
Using advanced computational genomic analysis of immune cells from mouse models, a researcher at the Pritzker School of Molecular Engineering (PME) at the University of Chicago and her collaborators discovered that, when exposed to a trigger, certain kinds of immune cells change their behavior in unexpected ways to produce the protein signals that cause lesions.