ArticleMedComm2024
PA28γ induces dendritic cell maturation and activates T-cell immune responses in oral lichen planus.
Article in MedComm, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
The trial behind it
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Who cites it
5 citing papers in PubMed.
- PA28γ-containing tumor-derived exosomes promote T-cell dysfunction in head and neck squamous cell carcinoma.Cellular & molecular immunology · 2026Article
- Heterogeneous mechanisms, risk stratification, and translational advances in the malignant transformation of oral potentially malignant disorders to oral squamous cell carcinoma.Frontiers in molecular biosciences · 2026Review
- PA28γ promotes the malignant progression of tumor by elevating mitochondrial function via C1QBP.eLife · 2025Article
- Etiopathogenesis of Oral Lichen Planus: A Review.Head and neck pathology · 2025Review
- PA28γ induces dendritic cell maturation and activates T-cell immune responses in oral lichen planus.MedComm · 2024Article
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oral lichen planus (OLP) is a common chronic inflammatory disease of the oral mucosa, the mechanism of its inflammatory progression has not yet been fully elucidated. PA28γ plays a significant role in a variety of immune-related diseases. However, the exact role of PA28γ in the pathogenesis of OLP remains unclear. Here, we demonstrated that PA28γ is overexpressed in epithelial cells and inflammatory cells of OLP tissues but has no significant relationship with OLP subtypes. Functionally, keratinocytes with high PA28γ expression could induce dendritic cell (DC) maturation and promote the T-cell differentiation into Th1 cells in response to the immune response. In addition, we found that a high level of PA28γ expression is associated with high numbers of infiltrating mature DCs and activated T-cells in OLP tissues. Mechanistically, keratinocytes with high PA28γ expression could promote the secretion of C-C motif chemokine (CCL)5, blocking CCL5 or/and its receptor CD44 could inhibit the induction of T-cell differentiation by keratinocytes with high PA28γ expression. In conclusion, we reveal that keratinocytes with high expression of PA28γ in OLP can induce DC maturation and promote T-cell differentiation through the CCL5-CD44 pathway, providing previously unidentified mechanistic insights into the mechanism of inflammatory progression in OLP.
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Registered trials
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