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Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils
Published on: January 21, 2020
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Th17-to-Tfh plasticity during periodontitis limits disease pathology
Flora A McClure1, Kelly Wemyss1, Joshua R Cox1
1Lydia Becker Institute of Immunology and Inflammation, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, The University of Manchester , Manchester, UK.
The Journal of Experimental Medicine
|May 31, 2024
Summary
Th17 cell plasticity, crucial in inflammation, was explored in periodontitis. Some Th17 cells shifted to Tfh cells in lymph nodes, a process limiting disease severity by enhancing oral immunity.
Area of Science:
- Immunology
- Microbiology
- Periodontal disease research
Background:
- Th17 cell plasticity is implicated in autoinflammatory diseases.
- Periodontitis involves Th17 cells, but their plasticity in this context is unknown.
Purpose of the Study:
- To investigate Th17 cell functional plasticity during periodontitis.
- To determine the role of Th17 cell plasticity in periodontitis pathology.
Main Methods:
- Utilized IL-17 fate-mapping in a periodontitis model.
- Analyzed T cell cytokine production and phenotype in gingiva and draining lymph nodes.
- Assessed the impact of Th17-to-Tfh plasticity on periodontal bone loss, IgG levels, and oral microbiota.
Main Results:
- Gingival Th17 cells largely retained IL-17A production during periodontitis.
- IL-17-expressing T cells in draining lymph nodes exhibited plasticity, differentiating into Tfh-like cells.
- This Th17-to-Tfh plasticity, dependent on IL-6, was protective, limiting bone loss and controlling oral commensal bacteria.
Conclusions:
- Th17 cell plasticity occurs in periodontitis, specifically a Th17-to-Tfh cell switch in lymph nodes.
- This plasticity serves a protective role by enhancing oral immunity and limiting periodontal disease.
- A subset of pathogenic Th17 cells can acquire a protective function through plasticity.

