What is it about?
Areca nut chewing impairs immune function in oral submucous fibrosis (OSF) by suppressing vital immune responses. It inhibits T-cell activation, lowers levels of cytokines like IL-2 and INF-γ, and promotes the differentiation of CD4+ T cells into regulatory T cells (Tregs), which further weaken cytotoxic T lymphocyte (CTL) activity and increase CD8+ T cell death. Additionally, it reduces neutrophil phagocytic activity and shifts immune cell balances, fostering an immunosuppressive environment that drives OSF progression. Myofibroblasts persist in fibrotic tissue by evading apoptosis through downregulating Fas receptors (critical for apoptosis) via TGF-β signaling and matrix stiffness. They also increase anti-apoptotic proteins like c-FLIP and secrete soluble FasL, shielding them from immune-mediated cell death and enabling continuous fibrosis. TGF-β is essential in OSF, converting CD4+ T cells into Tregs that secrete more TGF-β and IL-10, enhancing myofibroblast differentiation and reinforcing the fibrotic cycle. PD-L1 on myofibroblasts impacts CD4+ T cells in fibrotic regions by binding to their PD-1 receptors, reducing T-cell activation. This interaction changes CD4+ T cells from antifibrotic to profibrotic, increasing cytokines like IL-17A and TGF-β. This further promotes fibrosis and allows myofibroblasts to evade immune detection, contributing to persistent fibrotic tissue.
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Why is it important?
The article is important because it highlights the role of myofibroblasts and immune mechanisms in oral submucous fibrosis (OSF), a condition that can lead to serious health issues. Understanding how myofibroblasts evade cell death and how they interact with T cells can help researchers develop better treatments for OSF and similar fibrotic disorders. By uncovering these mechanisms, the article contributes to the broader knowledge of fibrosis and immune responses, which is crucial for improving patient care and outcomes.
Perspectives
This publication provides valuable insights into the complex interactions between myofibroblasts and the immune system in oral submucous fibrosis. It emphasizes the importance of understanding cellular mechanisms that contribute to disease progression, which could lead to innovative therapeutic strategies. Overall, the research underscores the need for a multidisciplinary approach in tackling fibrotic disorders, combining immunology and cellular biology for better patient management.
Professor Mohit Sharma
SGT Dental College Hospital & Research Institute
Read the Original
This page is a summary of: Myofibroblasts persist through immune privilege mechanisms to mediate oral submucous fibrosis: Uncovering the pathogenesis, Journal of Oral Biology and Craniofacial Research, November 2024, Elsevier,
DOI: 10.1016/j.jobcr.2024.10.008.
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