Atopic dermatitis (AD) is a complex inflammatory skin disorder influenced by immune dysregulation, barrier dysfunction, and pruritus. Key immune cells, including Th2 cells, ILC2s, and basophils, drive inflammation by releasing cytokines like IL-4, IL-5, IL-13, and IL-31, while alarmins such as TSLP, IL-25, and IL-33 amplify the response. These cytokines suppress barrier proteins like filaggrin, worsening the skin barrier. Effective treatments, including dupilumab and nemolizumab, have shown promise in reducing inflammation and pruritus. However, therapies targeting cytokines like IL-33, TSLP, IL-1α, IL-5, and IL-17 have shown limited efficacy in clinical trials, highlighting challenges in translating findings from animal models to human patients.

Pruritus is a hallmark symptom of AD, and IL-31 plays a significant role in this process, with nemolizumab offering relief in clinical studies. Chronic inflammation involves other cytokines, such as IL-22, which drives keratinocyte proliferation and thickening of the epidermis. Fezakinumab, an IL-22-targeting therapy, shows promise for severe AD. JAK inhibitors, including upadacitinib and abrocitinib, also offer promising results for moderate-to-severe AD.

Reference: Yamamura Y, Nakashima C, Otsuka A. Interplay of cytokines in the pathophysiology of atopic dermatitis: insights from Murin models and human. Front Med (Lausanne). 2024;11:1342176. doi: 10.3389/fmed.2024.1342176.