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Atopic dermatitis, prurigo nodularis, and chronic spontaneous urticaria are immune-mediated, inflammatory skin conditions characterized by intense itch and disease-specific skin lesions. Despite their different clinical presentations, the three diseases are unified by an aberrant type 2 immune response involving type 2 cytokines, immune cells, and sensory nerves that may underlie their shared clinical manifestations of inflammation and pruritus. The chronic nature of these conditions is associated with significant impairment in patients' quality of life and psychological disorders, such as anxiety and depression. This article reviews type 2 inflammation and its role in atopic dermatitis, prurigo nodularis, and chronic spontaneous urticaria, focusing on the pathophysiologic drivers of type 2 inflammation in each dermatologic condition. Understanding the shared immune mechanisms that underlie these seemingly distinct skin diseases and other concomitant inflammatory conditions is critical for applying therapeutic interventions targeting the type 2 immune pathway.
Chovatiya et al. (Sat,) studied this question.