ArticleThe Journal of experimental medicine2024
Th17-to-Tfh plasticity during periodontitis limits disease pathology.
Article in The Journal of experimental medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- The dynamic landscape of T helper cell plasticity and Th17-Treg instability in periodontitis.Experimental & molecular medicine · 2026Review
- Distinct spatial organization governs oral mucosal immunity.Nature immunology · 2026Article
- Divergent phenotypic and functional roles of human T follicular helper cells from infancy to adulthood.bioRxiv : the preprint server for biology · 2026Article
- Interleukin-17 in disease pathogenesis and therapy: recent advances in targeted drug design and medicinal chemistry.Frontiers in pharmacology · 2026Review
- Divergent T Cell Phenotypes Define Pediatric Crohn's Disease and Ulcerative Colitis.medRxiv : the preprint server for health sciences · 2025Article
- Mechanism of Lycium barbarum in treating periodontitis based on network pharmacology, molecular docking, and experimental validation.Clinical oral investigations · 2025Article
- Injectable cellular vesicle-based bone meal for inflammatory bone defect repair through restoring immune homeostasis.Theranostics · 2025Article
- Cytokines in gingivitis and periodontitis: from pathogenesis to therapeutic targets.Frontiers in immunology · 2024Review
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Authors and funding
12 authors.
Funding
Abstract
Th17 cell plasticity is crucial for development of autoinflammatory disease pathology. Periodontitis is a prevalent inflammatory disease where Th17 cells mediate key pathological roles, yet whether they exhibit any functional plasticity remains unexplored. We found that during periodontitis, gingival IL-17 fate-mapped T cells still predominantly produce IL-17A, with little diversification of cytokine production. However, plasticity of IL-17 fate-mapped cells did occur during periodontitis, but in the gingiva draining lymph node. Here, some Th17 cells acquired features of Tfh cells, a functional plasticity that was dependent on IL-6. Notably, Th17-to-Tfh diversification was important to limit periodontitis pathology. Preventing Th17-to-Tfh plasticity resulted in elevated periodontal bone loss that was not simply due to increased proportions of conventional Th17 cells. Instead, loss of Th17-to-Tfh cells resulted in reduced IgG levels within the oral cavity and a failure to restrict the biomass of the oral commensal community. Thus, our data identify a novel protective function for a subset of otherwise pathogenic Th17 cells during periodontitis.
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