ReviewJournal of oral biology and craniofacial research
Myofibroblasts persist through immune privilege mechanisms to mediate oral submucous fibrosis: Uncovering the pathogenesis.
Review in Journal of oral biology and craniofacial research. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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
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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Who cites it
4 citing papers in PubMed.
- cGAS-STING signaling in pollution-induced toxicity: mechanism and relieving medication.Apoptosis : an international journal on programmed cell death · 2026Review
- Pathological Interplay of ROS With Myofibroblasts: An Impediment to Corneal Restitution.Oxidative medicine and cellular longevity · 2026Review
- An organoid-guided roadmap for precision delivery of epigallocatechin gallate in oral submucous fibrosis.Frontiers in bioengineering and biotechnology · 2026Review
- Provoking myofibroblast death: Strategies to resolve fibrosis and remodel tumor microenvironment.World journal of clinical oncology · 2025Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immune privilege is the ability to tolerate foreign antigens without eliciting an inflammatory immune response. Several mechanisms explain a structure's immune privilege status, which is regulated by innate and adaptive immune responses. The role of myofibroblasts in perpetuating fibrosis by acquiring an immune privileged phenotype against the backdrop of oral submucous fibrosis (OSF) is evolving. Myofibroblasts persist through the Fas/FasL autocrine pathway and induce apoptosis in epithelial cells, explaining the juxtaposition of apoptotic cells in areas of fibrosis. However, increased matrix stiffness, in addition to activating TGF-β, reduces Fas surface expression in myofibroblasts, increasing their resistance to apoptosis. The reciprocal amplification loop between the immune checkpoint proteins programmed death-ligand 1 (PD-L1) and TGF-β involves the YAP-TAZ and SMAD2,3 pathways and dramatically enhances profibrotic signalling. Increased matrix stiffness also enhances cMYC expression, which subsequently amplifies PD-L1 levels on myofibroblasts. The increase in PD-L1 on the myofibroblast microengineers the phenotype of CD4
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Registered trials
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