ArticleFrontiers in immunology2025
Activation of NF-κB signaling in tissue-resident memory T cells promotes recurrent psoriasis in mice.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Hepatic drug transporters in pharmacotherapy: mechanisms, therapeutic targeting, and clinical translation.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Molecular Signature and miRNA Pattern of CD4 + T Lymphocytes in Plaque Psoriasis.Clinical reviews in allergy & immunology · 2026Review
- Reprogramming immunometabolism: linking nutrient sensing, cell death, and therapeutic innovation.Immunologic research · 2026Review
- Shikonin-Loaded ROS-Responsive Microneedles for Psoriasis Therapy: Formulation, Transdermal Delivery, and Mechanistic Evaluation.Pharmaceutics · 2026Article
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Authors and funding
11 authors.
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Abstract
Background: Recurrence triggered by immunological memory is a critical challenge in the treatment of psoriasis. Tissue-resident memory T (Trm) cells are the primary pacemakers in recurrent psoriasiform dermatitis following stimulation and infection by previous pathogens. However, the mechanisms underlying Trm cell activation remain unclear. Methods: In this study, imiquimod-induced recurrent psoriatic mice were established to characterize the phenotypes of different Trm cell subsets. CD8 Results: Mice displayed severe psoriatic dermatitis after repeated imiquimod treatment. The CD8 Conclusion: Together, these findings suggest that canonical and non-canonical NF-κB signaling directly activates Trm cell differentiation, inhibits cellular cuproptosis, and promotes recurrent psoriasis.
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