Experimental & Molecular Medicine· 2026Q1· Review
The dynamic landscape of T helper cell plasticity and Th17–Treg instability in periodontitis
- 0citations
- Q1SCImago
- 2026year
Short summary
Periodontitis immune response is driven by unstable, plastic T helper cells, not just static subsets, with evidence of IL-17+ Tregs indicating maladaptive transitions that cause chronic tissue destruction.
AI-generated from the title and abstract; the full text is not read.
Key points
- Periodontitis tissue destruction stems from an exaggerated host immune response, particularly involving CD4+ T helper cell subsets.
- Immune imbalance and functional instability, rather than a single dominant T cell lineage, drive periodontitis.
- T helper cell plasticity, including the emergence of IL-17+ Treg cells, is a key feature of the disease.
- Maladaptive transitions in T cell phenotypes contribute to chronic tissue destruction in periodontal lesions.
AI-generated from the title and abstract; the full text is not read.
Abstract
Abstract Periodontitis is a chronic inflammatory disease initiated by a dysbiotic microbiome, yet tissue destruction is primarily driven by an exaggerated host immune response. CD4⁺ T helper (Th) cell subsets play important roles in regulating periodontal inflammation and osteoclast-mediated bone resorption through distinct cytokine networks. Th1 and Th17 responses are closely associated with pro-inflammatory signaling and alveolar bone loss, whereas Th2 and regulatory T (Treg) cells exert context-dependent immunomodulatory functions. Beyond these subsets, Th9 and Th22 cells further expand the complexity of T cell-mediated regulation in periodontal lesions. Importantly, accumulating evidence supports T helper cell plasticity, exemplified by the emergence of IL-17⁺ Treg, suggesting that periodontal disease reflects immune imbalance and functional instability rather than the dominance of a single lineage. Clarifying these mechanisms may support the development of targeted immunomodulatory strategies aimed at restoring oral mucosal immune homeostasis. This review shifts the focus from static T cell subsets to their dynamic phenotypic flexibility, highlighting how maladaptive transitions drive chronic tissue destruction.
The authors' abstract, as published at the source. Experimental & Molecular Medicine, 2026 · DOI ↗
Continue with a free account
Ask the paper: 3 free questions a day about this paper; save it, get its citation, new summaries every day for your field. Takeaways are Premium.
Continue free on the webSign in with Google or Apple; no card needed. You come back to this paper.
On your phone:
Field: Periodontics
PeriodonticsDentistry