LAUSR

(842 pg/mL and 1,356 pg/mL, respectively). The patient showed good compliance with 4 mg/day baricitinib treatment, without any relapse or adverse events. The EASI score remained 5 until 52 weeks, and DLQI, P-NRS, and ADCT scores all remained 0 during this period. AD is a common inflammatory skin disease characterized by chronic, eczematous, and pruritic skin lesions caused by skin barrier dysfunction [1]. Cytokines from T helper (Th) 2 cells, such as interleukin (IL)-4, IL-13, and IL-31, play critical roles in the pathogenesis of AD [1]. Although clinical research has revealed that both the anti-IL-4 receptor antibody, dupilumab, and JAK inhibitors, including baricitinib, significantly mitigate the symptoms of AD, very few studies have reported an inadequate response to dupilumab [2, 3]. Moreover, no report has described the contrasting therapeutic effects of dupilumab and baricitinib. The pathogenesis of AD is not exclusively explained by Th2 immunity, with Th1, Th17, and Th22 cells contributing to AD disease heterogeneity [4]. Cytokines secreted from nonTh2 cells, such as IL-22, IL-23, and interferon, are not inhibited by dupilumab, however, as the effect of all these cytokines is mediated by the JAK 1/2 signalling pathway, these cytokines may be blocked by baricitinib. The failure of dupilumab in the present case may be due to its insufficient dose for a long enough period. However, the contrasting therapeutic results observed probably indicate a significant contribution of these non-type 2 cytokines. In Japan, both dupilumab and JAK inhibitors are used as systemic therapies for moderate-to-severe AD. However, no clear criteria have been proposed for their use. Notably, Asian patients with AD have much higher expression levels of Th22 and Th17 cell-related cytokines in lesional skin compared to patients of European ancestry [5]. In AD patients with prominent lichenification or epidermal acanthosis, which suggest a major role of non-type 2 cytokines, for example, Asian AD or the prurigo phenotype of AD, JAK inhibitors may be more suitable than dupilumab considering their effectiveness in also suppressing non-type 2 cytokines.