ArticleBMC research notes2026
Bcl-3 expression in the imiquimod-induced psoriasis mouse skin.
Article in BMC research notes, 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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8 authors.
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Abstract
objectivePsoriasis is an inflammatory process in the skin involving the loss of normal function of immune cells and keratinocytes. TNF-α is a pro-inflammatory cytokine involved in psoriasis induced by NF-κB activation. In contrast, the anti-inflammatory cytokine IL-10 can suppress macrophage TNF-α production. The non-classical NF-κB regulator, Bcl-3, can regulate IL-10 expression. Limited knowledge exists on Bcl-3 and IL-10 expression in psoriasis and their action on TNF-α. This study evaluated Bcl-3, TNF-α, and IL-10 expression levels in mouse skin in a model of imiquimod-induced psoriasis.
resultsFemale Balb/c mice were shaved in the lumbar region and administered 62 mg of 5% imiquimod (IMQ) cream for six consecutive days. The non-lesional group received only 62 mg of cream without IMQ for six consecutive days. RT-qPCR was used to determine Bcl-3, TNF-α, and IL-10 expression. Imiquimod psoriasis induction was confirmed phenotypically and histologically. On day 2 of imiquimod treatment, the lesioned skin significantly reduced the expression level of Bcl-3, and TNF-α. However, on day 6, a significant difference in the expression of Bcl-3 (sixfold), TNF-α (twofold), and IL-10 (threefold) was found in lesioned skin compared to non-lesioned skin. Results suggest that late-stage overexpression of Bcl-3 in lesioned skin induces IL-10 expression to regulate TNF-α inflammatory effects.
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