Interleukin‐35 inhibits alveolar bone resorption by modulating the Th17/Treg imbalance during periodontitis

Aim T lymphocytes play a central role during the pathogenesis of periodontitis, and the imbalance between the pathogenic T‐helper type 17 (Th17) and protective T‐regulatory (Treg) lymphocytes determines the tooth‐supporting alveolar bone resorption. Interleukin (IL)‐35 is a novel anti‐inflammatory cytokine with therapeutic properties in diseases whose pathogenesis is associated with the Th17/Treg imbalance; however, its role during periodontitis has not been established yet. This study aimed to elucidate whether IL‐35 inhibits the alveolar bone resorption during periodontitis by modulating the Th17/Treg imbalance. Materials and Methods Mice with ligature‐induced periodontitis were treated with locally or systemically administrated IL‐35. As controls, periodontitis‐affected mice without IL‐35 treatment and non‐ligated mice were used. Alveolar bone resorption was measured by micro‐computed tomography and scanning electron microscopy. The Th17/Treg pattern of the immune response was analysed by qPCR, ELISA, and flow cytometry. Results IL‐35 inhibited alveolar bone resorption in periodontitis mice. Besides, IL‐35 induced less detection of Th17 lymphocytes and production of Th17‐related cytokines, together with higher detection of Treg lymphocytes and production of Treg‐related cytokines in periodontitis‐affected tissues. Conclusion IL‐35 is beneficial in the regulation of periodontitis; particularly, IL‐35 inhibited alveolar bone resorption and this inhibition was closely associated with modulation of the periodontal Th17/Treg imbalance.