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<p>Bullous pemphigoid, chronic spontaneous urticaria, prurigo nodularis, and chronic prurigo of unknown origin are distinct chronic skin diseases with a high disease burden and an ongoing need for safe and effective therapies. Advances in our understanding of disease mechanisms have highlighted convergent type 2-associated neuroimmune pathways that may contribute to chronic itch and skin lesions across these conditions. In bullous pemphigoid, autoantibody binding of two dermal–epidermal junction proteins followed by complement system activation shapes the local immune environment to favor T helper cell 2 polarization and perpetuation of type 2 inflammation. In chronic spontaneous urticaria, mast cell activation and downstream mediators, including type 2 cytokines, may contribute to amplification of inflammation and itch. In prurigo nodularis, chronically activated itch sensory neurons induce an itch-scratch cycle with T-cell activation in parallel to mast cell degranulation, resulting in neurogenic inflammation that sustains the itch-scratch cycle. The pathogenesis of chronic prurigo of unknown origin is not well understood, but evidence to date points to interactions between skin barrier defects and immune and neural dysregulation triggering T helper cell 2 polarization. In this review, we discuss the role of type 2 inflammation in bullous pemphigoid, chronic spontaneous urticaria, prurigo nodularis, and chronic prurigo of unknown origin, and how this understanding is currently translated into new targeted therapeutic options.</p>

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Shared Mechanistic Pathways in Bullous Pemphigoid, Chronic Spontaneous Urticaria, Prurigo Nodularis, and Chronic Prurigo of Unknown Origin: Implications for Targeted Therapies

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月24日

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  • Enno Schmidt,
  • Marta Ferrer Puga,
  • Brian S. Kim,
  • Eric L. Simpson

摘要

Bullous pemphigoid, chronic spontaneous urticaria, prurigo nodularis, and chronic prurigo of unknown origin are distinct chronic skin diseases with a high disease burden and an ongoing need for safe and effective therapies. Advances in our understanding of disease mechanisms have highlighted convergent type 2-associated neuroimmune pathways that may contribute to chronic itch and skin lesions across these conditions. In bullous pemphigoid, autoantibody binding of two dermal–epidermal junction proteins followed by complement system activation shapes the local immune environment to favor T helper cell 2 polarization and perpetuation of type 2 inflammation. In chronic spontaneous urticaria, mast cell activation and downstream mediators, including type 2 cytokines, may contribute to amplification of inflammation and itch. In prurigo nodularis, chronically activated itch sensory neurons induce an itch-scratch cycle with T-cell activation in parallel to mast cell degranulation, resulting in neurogenic inflammation that sustains the itch-scratch cycle. The pathogenesis of chronic prurigo of unknown origin is not well understood, but evidence to date points to interactions between skin barrier defects and immune and neural dysregulation triggering T helper cell 2 polarization. In this review, we discuss the role of type 2 inflammation in bullous pemphigoid, chronic spontaneous urticaria, prurigo nodularis, and chronic prurigo of unknown origin, and how this understanding is currently translated into new targeted therapeutic options.