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- Campus Sanofi
- Jun 11, 2024
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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

Atopic dermatitis (AD) is a chronic, immune-mediated inflammatory disease that often begins in early infancy and persists into adulthood.1-3 While symptoms such as the intense itch that disrupts the lives of patients are well known, AD also imposes a profound chronic ‘hidden burden’ that extends far beyond visible skin lesions, significantly impairing patients' mental health, relationships, and daily productivity.1-11 This burden can be compounded by the treatment regimens themselves, which can be time-consuming, economically straining, and limited by low patient satisfaction and patient phobias of treatments and their side effects.12-14