This website contains promotional content and is intended for Healthcare Professionals based in the United States only.
Atopic dermatitis (AD) is a chronic inflammatory heterogenous skin condition marked by immune dysregulation and impaired skin barrier function.1,2 For healthcare professionals seeking to understand the immunologic drivers of AD, the OX40L signaling axis has emerged as a key pathway involved in T-cell activation and chronic inflammation.2,3
Atopic dermatitis (AD) is a chronic inflammatory condition caused by complex underlying pathophysiology, driven by genetic, immunologic and environmental factors and triggers that collectively disrupt the epidermis.1-3 Despite the range of treatment options available, patients continue to experience fluctuations in disease activity due to the heterogeneity of AD.4-6 There remains an unmet need to develop a deeper understanding of the diverse immune dysregulation profiles found in patients with AD and determine optimal treatment on a more personalized basis.4,6
Atopic dermatitis (AD) is a heterogenous disease defined by contributions from multiple distinct inflammatory pathways.1 Although type 2 inflammation‘s role in AD pathogenesis is well-characterized, other non-type 2 T cell-mediated pathways also play a role in AD chronicity.1,2 For healthcare professionals seeking to understand the diversity of immune signatures in their AD patients, looking beyond Th2 cytokines is essential.1
