Chovatiya Raj, Hawkes Jason E, DiRuggiero Douglas, Pansch Leigh Ann, Simcox Elizabeth, Gonzalez Tayler
Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois, USA.
Center for Medical Dermatology and Immunology Research, Chicago, Illinois, USA.
Int J Dermatol. 2025 Jun;64(6):978-991. doi: 10.1111/ijd.17707. Epub 2025 Mar 22.
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.
特应性皮炎、结节性痒疹和慢性自发性荨麻疹是免疫介导的炎症性皮肤病,其特征为剧烈瘙痒和特定疾病的皮肤损害。尽管这三种疾病临床表现不同,但它们都由涉及2型细胞因子、免疫细胞和感觉神经的异常2型免疫反应所统一,这可能是它们炎症和瘙痒共同临床表现的基础。这些疾病的慢性性质与患者生活质量的显著受损以及焦虑和抑郁等心理障碍相关。本文综述了2型炎症及其在特应性皮炎、结节性痒疹和慢性自发性荨麻疹中的作用,重点关注每种皮肤病中2型炎症的病理生理驱动因素。了解这些看似不同的皮肤疾病以及其他伴随炎症性疾病背后的共同免疫机制,对于应用针对2型免疫途径的治疗干预措施至关重要。