Racial and ethnic disparities in T helper 2-mediated inflammatory skin disorders.

T helper type 2 (Th2)-mediated inflammatory skin diseases, including atopic dermatitis, discoid lupus erythematosus, systemic sclerosis, autoimmune bullous diseases and secondary lymphoedema, demonstrate significant racial and ethnic disparities in prevalence, severity and clinical outcomes. These disorders share pathogenic mechanisms involving Th2-driven immune activation, fibrosis and epidermal barrier dysfunction, leading to chronic inflammation and substantial morbidity. Black and Hispanic populations consistently experience greater disease burden, more severe clinical manifestations and reduced quality of life compared with White patients, reflecting complex interactions between biologic and socioeconomic factors. Current molecular and immunological studies suggest that ancestry-associated differences in immune polarization, cytokine signalling, autoantibody expression, fibrotic pathways and epidermal barrier biology may contribute to variation in disease phenotype and severity across Th2-mediated disorders. Black patients have demonstrated enhanced Th2 and Th22-mediated inflammation, increased IgE production, elevated interleukin (IL)-4, IL-13 and IL-22 signalling, and distinct genetic and serological profiles, including variation in filaggrin-related barrier proteins and autoantibody expression. However, mechanistic studies directly evaluating race-associated Th2 immune responses remain limited in many inflammatory skin diseases, and under-representation of diverse populations in translational research and clinical trials continues to restrict understanding of disease biology and therapeutic response. This review synthesizes the current epidemiological, molecular and immunological evidence linking race, immune dysregulation and disease heterogeneity across Th2-mediated skin disorders. Together, these findings support a growing framework in which ancestry-associated differences in immune regulation and social determinants jointly shape disparities in Th2-mediated inflammatory skin disease.

Abstract from PubMed