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Translational research has changed the understanding of atopic dermatitis (AD) pathogenesis beyond the basic mechanisms of immunology. The study in patients of rational therapies based on targeted therapies (biologicals) provides valuable information from the patient and provides lessons of clinical immunology on clinically relevant mechanism of AD pathogenesis. AD features such as skin barrier defect, skin dysbiosis, and pruritus share a common abnormal adaptive immune response process. Skin-homing CLA+CD4+ memory T-cells produce IL-4, IL-13, and IL-31 which are key mediators in AD pathogenesis. Lessons learned from AD show that translational immunology allows generating rational therapies for AD and learning its immunopathogenesis in the patient.