similar trends (significant at wks 2 and 8 vs baseline) with UPA 30mg dose. There were no clear trends in Th17 cytokine levels (IL-17A, IL-17F, or CCL20). Baseline levels of AEC significantly correlated with baseline EASI (r¼0.39, P<0.0001); in addition, percentage change from baseline to wk 16 in AEC correlated with percentage change at wk 16 in EASI (r¼0.62, P<0.0001) and pruritus NRS (r¼0.66, P<0.0001). Baseline serum levels of Th2 and Th22 cytokines significantly correlated with baseline EASI scores (CCL17/18/26: r¼0.44/0.43/0.41, P<0.0001; IL-22: r¼0.43, P<0.001). Changes from baseline to wk 16 in Th2 and Th22 cytokines correlated with percentage changes in EASI (CCL18/26: r¼0.58/ 0.57, P<0.0001; IL-22: r¼0.48, P<0.0001) and pruritus NRS (CCL18/26: r¼0.37/0.43, P<0.01; IL-22: r¼0.38, P<0.001). While baseline levels of serum total IgE correlated with baseline EASI (r¼0.35, P<0.001), no trends in allergen-specific or total IgE levels as a function of study duration were observed. DISCUSSION Eosinophil counts and serum levels of Th2 (CCL18/26) and Th22 (IL-22)-attracting chemokines were significantly reduced with UPA treatment (15/ 30mg) as early as wk 2, suggesting UPA may have early and robust effects on Th2, Th22, and eosinophil axes. No significant changes in total and specific IgE levels were observed, suggesting that UPA clinical efficacy is independent of IgE levels, and this observation coupled with the lack of clinical efficacy for anti-IgE strategies in patients with AD argues against the primary role of IgE in AD pathogenesis.