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Atopic dermatitis (AD), prurigo nodularis (PN), chronic spontaneous urticaria (CSU), and bullous pemphigoid (BP) look strikingly different on the skin: eczematous plaques, nodules, transient wheals, blisters. Beneath those differences, each can involve components of Type 2 inflammation. Across five short videos, faculty move from what clinicians see to the immune network underneath, including the distinct and overlapping roles of IL-4 and IL-13, and then consider what that biology means for treatment. Shared biology does not mean identical disease, but recognizing where these conditions connect can sharpen how clinicians understand each one.
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