ArticleMediators of inflammation2026
Luteolin Disrupts Keratinocyte-Dendritic Cell Communication in Psoriasis by Targeting Rh Family C Glycoprotein.
Article in Mediators of inflammation, 2026. 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.
- Luteolin Disrupts Keratinocyte-Dendritic Cell Communication in Psoriasis by Targeting Rh Family C Glycoprotein.Mediators of inflammation · 2026Article
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10 authors.
Funding
Abstract
Psoriasis, a chronic inflammatory skin disease, arises from a dysregulated interaction between keratinocytes (KCs) and dendritic cells (DCs). We previously identified Rh family C glycoprotein (RHCG) as a key mediator of KC inflammation and DC activation. Here, we demonstrate that luteolin, a bioactive compound derived from the traditional Chinese formula cooling blood and detoxicating formula (CBDF), directly binds to RHCG, as confirmed by multiple computational methods and in vitro experiments. In vitro, luteolin suppressed RHCG expression in KCs, reducing CXCL14 secretion and subsequent DC activation. Spatial transcriptomics (STs) revealed that luteolin preferentially targets DC-enriched spatial domains and restores desmosomal protein expression (e.g., DSC2), which is dysregulated in psoriasis. In vivo, luteolin ameliorated psoriasis-like inflammation in imiquimod-induced mice, lowering Psoriasis Area and Severity Index (PASI) scores and normalizing pathological markers. Our findings indicate that luteolin disrupts KC-DC communication through multiple modes of action, thereby reversing tissue-level pathology and demonstrating its potential as a targeted therapy for psoriasis.
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