ArticleLife sciences2025
Type I interferon protects against bone loss in periodontitis by mitigating an interleukin (IL)-17-neutrophil axis.
Article in Life sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Interferon-JAK-STAT Axis in Bone Metabolism.Current osteoporosis reports · 2026Review
- CD169Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Ferroptosis and macrophage efferocytosis in periodontitis: Biological insights and therapeutic advances.Virulence · 2025Review
- Oral stem cells in combination with hydrogels as biomimetic bioactive platforms for periodontal tissue engineering.Frontiers in oral health · 2025Review
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Authors and funding
14 authors.
Funding
Abstract
Type I interferons (IFNs-I), a group of pleiotropic cytokines, critically modulate host response in various inflammatory diseases. However, the role of the IFN-I pathway in periodontitis remains largely unknown. In this report, we describe that the IFN-β levels in the gingival crevicular fluid of human subjects were negatively associated with periodontitis and clinical gingival inflammation. Disruption of IFN-I signaling worsened alveolar bone resorption in a ligature-induced periodontitis murine model. Deficiency of the IFN-I pathway resulted in an exaggerated inflammatory response in myeloid cells and drastically increased the interleukin-17 (IL-17)-mediated neutrophil recruitment in the gingiva. We further identified that the myeloid lineage-specific IFN-I response was essential in safeguarding against periodontal inflammation by suppressing the IL-17-producing γδ T cells in gingiva. IFN-I signaling also directly repressed osteoclastogenesis in monocytes, which are precursor cells for osteoclasts. Therefore, our findings demonstrate that an integral myeloid-specific IFN-I pathway protects against bone loss by keeping the IL-17-neutrophil axis in check and directly inhibiting osteoclast formation in periodontitis.
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Registered trials
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