ReviewFrontiers in immunology2026
NF-κB-c-Rel in psoriasis: genetic susceptibility, immunopathogenic circuits, and emerging therapeutic opportunities.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Authors and funding
6 authors.
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Abstract
Psoriasis is a chronic, relapsing, immune-mediated inflammatory dermatosis characterized by aberrant keratinocyte hyperproliferation and prominent infiltration of inflammatory leukocytes. Among the NF-κB transcription factor family, c-Rel is the first member conclusively implicated as a psoriasis susceptibility gene, and its dysregulated expression positively correlates with clinical disease activity. Mechanistically, c-Rel orchestrates pathogenic inflammation by coordinating immune-cell differentiation programs and inflammatory cytokine production, while also contributing to keratinocyte proliferation and inflammatory responses in non-hematopoietic compartments. Emerging therapeutic approaches that modulate c-Rel, ranging from biologics and small-molecule inhibitors to nucleic-acid-based interventions, have shown encouraging efficacy in both clinical study and experimental psoriasis models. However, key translational hurdles remain, including suboptimal delivery, incomplete target-cell specificity, and long-term safety concerns. Deeper delineation of upstream activation cues and cell-type-restricted c-Rel regulatory circuits will be essential to enable precision targeting of c-Rel in psoriasis.
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