Spongiotic Psoriasiform Dermatitis with Dual Features of Eczema and Psoriasis: JAK Inhibition as a Potential Therapeutic Option

Psoriasis and eczema are inflammatory skin disorders with distinct immune mechanisms. Psoriasis is mainly driven by Th17 immune responses, while eczema, notably atopic dermatitis (AD), is Th2-mediated. Spongiotic psoriasiform dermatitis (SD/PSO), a hybrid phenotype of both, lacks precise immunophenotypic characterization and treatment strategies. Existing studies have shown that some SD/PSO patients exhibit 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. To characterize the immunological and differentiation profiles of SD/PSO, clarify their differences from classic psoriasis and AD, and identify alternative therapies for conventional therapy-resistant patients. Four SD/PSO cases were evaluated. Histopathological analysis and TSA-based multiplex immunofluorescence assay were performed to assess immune profiles and keratinocyte differentiation profiles. In four SD/PSO patients, conventional therapies showed inadequate response, and three cases experienced lesion exacerbation with IL-17A inhibitors. Immunomarker analysis revealed mixed Th17/Th2 activation: Th17 markers (IL-17A, IL-23, IL-36A/G) were comparably elevated to psoriasis, while IL-4 levels matched AD and IL-13 exhibited moderate-level expression (between PSO and AD). SD/PSO lesions exhibited psoriasis-like epidermal differentiation with JAK-STAT hyperactivation, and JAK inhibitor treatment induced significant clinical improvement. SD/PSO represents a mixed AD-PSO immunophenotype with psoriasis-like differentiation patterns, characterized by co-activated Th17/Th2 pathways and JAK-STAT hyperactivation. JAK inhibitors effectively treat SD/PSO patients 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.