ArticleScientific reports2025
Alloferon and IL-22 receptor expression regulation on the pathogenesis of imiquimod-induced psoriasis.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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Who cites it
1 citing paper in PubMed.
- A review of core immuno-inflammatory mechanisms and key regulatory targets in psoriasis.American journal of clinical and experimental immunology · 2026Review
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8 authors.
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Abstract
Psoriasis is an immune-mediated inflammatory skin disease. IL-22, a proinflammatory cytokine, is implicated in psoriasis pathogenesis; however, there is currently no established biological treatment targeting IL-22 or its receptor, IL-22Rα. Alloferon is a short peptide that has an antiinflammatory effect on skin disorders; however, little is known about its anti-inflammatory activity in psoriasis. We investigated the regulatory role of alloferon in the development of psoriasis in an imiquimod (IMQ)-induced psoriasis model through the regulation of IL-22Rα expression. The expression of IL-22Rα was analyzed by immunofluorescence staining in primary human keratinocytes. The effect of alloferon on the development of psoriasis was investigated in IMQ-induced wild-type and IL-22Rα KO mice. We found that alloferon decreased the expression of IL-22Rα in psoriasis-like keratinocytes treated with TNF-α, while epidermal hyperplasia was observed in IMQ-induced wild-type and IL-22Rα KO mice. In addition, the expression of IL-1β, IL-19, and IL-33 was suppressed when IL-22Rα KO mice were treated with alloferon. The findings of this study indicate that alloferon could be an effective potential drug for the treatment of psoriasis by interrupting IL-22 signaling and factors related to skin inflammation.
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