Targeting type 2 Inflammation in bullous pemphigoid: Exploring the novel role of upstream tslp and IL-33 as therapeutic targets

Summary: Abstract Body: This study explores the theoretical potential of targeting thymic stromal lymphopoietin (TSLP) and interleukin-33 (IL-33) to modulate inflammation in bullous pemphigoid (BP). Conventional therapies such as methotrexate, mycophenolate mofetil, and systemic corticosteroids have limitations in their efficacy and adverse event profile. Recent breakthroughs have demonstrated the importance of type 2 inflammation in bullous pemphigoid. A review of current literature and analysis of cytokine pathways in type 2 inflammatory conditions such as atopic dermatitis and asthma, we evaluated the roles of TSLP and IL-33 in the pathogenesis of BP. The therapeutic targeting of these cytokines in related type 2 diseases underscores their promise in BP. Targeting of TSLP or IL-33 alter the inflammatory milieu to inhibit IL-4, IL-5, IL-13, IgE, CCL17 (TARC), & CCL22 (MDC) production, which have all been implicated in the pathogenesis of BP. These findings highlight the potential for targeting TSLP and IL-33 as innovative therapeutic strategies in BP, offering a novel approach to addressing type 2 inflammation in this disease. Therapeutic targeting of these upstream cytokines result in greater efficacy, lower risk of systemic side effects, and improved patient outcomes in BP versus conventional therapies. Tammy E. Ehimwenma-Point Du Jour¹, Gabriela Soto-Canetti², Jordan Talia² 1. Meharry Medical College, Nashville, TN, United States. 2. Mount Sinai Health System, New York, NY, United States. Clinical Research: Interventional Research