Clinical and experimental dermatology · 2025
Spongiotic psoriasiform dermatitis with dual features of eczema and psoriasis: Janus kinase inhibition as a potential therapeutic option.
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Cheng Wenjie, Pan Chaolan, Xu Qianyue, Li Jiawen, Wang Xiaoxiao, Wang Yumeng, Sun Peiyi, Chen Xuanyi, Yang Jinxiang, Yao Zhirong, Li Chunxiao
Аннотация
BACKGROUND: Psoriasis (PSO) and eczema are inflammatory skin disorders with distinct immune mechanisms. PSO is mainly driven by T helper (Th)17 immune responses, while eczema, notably atopic dermatitis (AD), is Th2 mediated. Spongiotic psoriasiform dermatitis (SD/PSO), a hybrid phenotype of both conditions, lacks precise immunophenotypic characterization and specific treatment strategies. Existing studies have shown that some patients with SD/PSO exhibit a poor response to conventional and single T-cell axis-targeted therapies (such as Th2/Th17 inhibitors), suggesting cross-activation of immune pathways, which urgently requires more targeted intervention strategies.
OBJECTIVE: To characterize the immunological and differentiation profiles of SD/PSO, clarify its differences from classical PSO and AD, and identify alternative therapies for conventional therapy-resistant patients.
METHODS: Four patients with SD/PSO were evaluated. Histopathological analysis and tyramide signal amplification-based multiplex immunofluorescence assay were performed to assess immune profiles and keratinocyte differentiation profiles.
RESULTS: In four patients with SD/PSO, conventional therapies showed inadequate response. Three patients experienced lesion exacerbation with interleukin (IL)-17A inhibitors. Immunomarker analysis revealed mixed Th17/Th2 activation: Th17 markers (IL-17A, IL-23, IL-36A/G) were comparably elevated to PSO, while IL-4 levels matched AD and IL-13 exhibited moderate-level expression (between PSO and AD). SD/PSO lesions exhibited PSO-like epidermal differentiation with Janus kinase-signal transducer and activator of transcription (JAK-STAT) hyperactivation and JAK inhibitor treatment induced significant clinical improvement.
CONCLUSIONS: SD/PSO represents a mixed AD-PSO immunophenotype with PSO-like differentiation patterns, characterized by coactivated Th17/Th2 pathways and JAK-STAT hyperactivation. JAK inhibitors effectively treat patients with SD/PSO by suppressing multi-T-cell axis-targeted inflammatory signals and blocking epidermal hyperproliferation, establishing JAK-STAT inhibition as a targeted strategy. Larger studies are needed to validate results and explore combination therapies.
OBJECTIVE: To characterize the immunological and differentiation profiles of SD/PSO, clarify its differences from classical PSO and AD, and identify alternative therapies for conventional therapy-resistant patients.
METHODS: Four patients with SD/PSO were evaluated. Histopathological analysis and tyramide signal amplification-based multiplex immunofluorescence assay were performed to assess immune profiles and keratinocyte differentiation profiles.
RESULTS: In four patients with SD/PSO, conventional therapies showed inadequate response. Three patients experienced lesion exacerbation with interleukin (IL)-17A inhibitors. Immunomarker analysis revealed mixed Th17/Th2 activation: Th17 markers (IL-17A, IL-23, IL-36A/G) were comparably elevated to PSO, while IL-4 levels matched AD and IL-13 exhibited moderate-level expression (between PSO and AD). SD/PSO lesions exhibited PSO-like epidermal differentiation with Janus kinase-signal transducer and activator of transcription (JAK-STAT) hyperactivation and JAK inhibitor treatment induced significant clinical improvement.
CONCLUSIONS: SD/PSO represents a mixed AD-PSO immunophenotype with PSO-like differentiation patterns, characterized by coactivated Th17/Th2 pathways and JAK-STAT hyperactivation. JAK inhibitors effectively treat patients with SD/PSO by suppressing multi-T-cell axis-targeted inflammatory signals and blocking epidermal hyperproliferation, establishing JAK-STAT inhibition as a targeted strategy. Larger studies are needed to validate results and explore combination therapies.