ReviewClinical and experimental dental research2025
FOXP3+ T Cells-An Emerging Evidence in Periodontitis Therapeutics.
Review in Clinical and experimental dental research, 2025. 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.
- Regulatory T Cells in Peri-implant Diseases: Current Osteoimmunologic Perspectives and Translational Challenges.Tissue engineering and regenerative medicine · 2026Review
- Mechanisms of the IL-33/ST2 Signaling Axis in Regulating Bone Metabolism.Biomolecules · 2026Review
- The role of the neuro-immune-bone axis in osteoporosis: from bone remodeling imbalance to multi-system interactions.Frontiers in immunology · 2026Review
- Tregs and persistentFrontiers in oral health · 2026Article
- FOXP3+ T Cells-An Emerging Evidence in Periodontitis Therapeutics.Clinical and experimental dental research · 2025Review
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo review interaction of FOXP3+ regulatory T cells with Th17 cells in determining the progression of periodontitis. MATERIAL AND METHODOLOGY: Literature review pertaining to FOXP3+ regulatory T cells, Th17 cells, and periodontitis was analyzed. Descriptive summary is presented.
resultsFOXP3+ regulatory T cells (Tregs) play an essential role in maintaining immune homeostasis and modulating inflammatory responses. The balance between Tregs and pro-inflammatory Th17 cells is crucial in determining the progression of periodontitis, a chronic immune-mediated inflammatory disease. While Tregs are responsible for suppressing excessive immune activation and preventing tissue destruction, an imbalance favoring Th17 cells leads to increased osteoclastic activity and alveolar bone loss through IL-17 and RANKL signaling. The inflammatory microenvironment in periodontitis compromises FOXP3+ Treg stability and function, thereby allowing unregulated immune responses that exacerbate periodontal tissue breakdown. Recent studies suggest that strategies aimed at enhancing Treg-mediated immune regulation, such as IL-2 supplementation, all-trans retinoic acid (ATRA), IL-33 administration, and CCL22-mediated recruitment, could mitigate periodontal inflammation and preserve alveolar bone integrity. Furthermore, systemic conditions like diabetes and obesity play a significant role in disrupting Treg function by promoting a pro-inflammatory environment, impairing immune regulation, and exacerbating immune dysregulation. This dysfunction weakens the protective role of Tregs, leading to an intensified inflammatory response that accelerates periodontal tissue destruction and alveolar bone loss.
conclusionUnderstanding the mechanisms governing FOXP3+ Treg stability and their interaction with pathogenic Th17 responses is essential for developing targeted immunomodulatory therapies. Future research should focus not only on selectively expanding Tregs but also on translational strategies such as adoptive Treg transfer and IL-17 inhibition, while carefully balancing efficacy and the risk of systemic immunosuppression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.