Regulatory B cells induced by interleukin-35 inhibit inflammation and alveolar bone resorption in ligature-induced periodontitis.

BACKGROUND: Regulatory B cells (Bregs) have been reported to suppress immune responses and alveolar bone loss in murine periodontitis models. These cells could be induced by interleukin-35 (IL-35) which is increased upon periodontal inflammation. Thus, this study aimed to explore the role of Bregs induced by IL-35 in periodontitis.

METHODS: Experimental periodontitis was induced in mice by ligature. Two weeks after ligation, the test group was systemically treated with IL-35 for one week. Four weeks after ligation, all mice were sacrificed and alveolar bone loss was evaluated by micro-computed tomography (micro-CT). Cytokines associated with periodontitis were analyzed using reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and enzyme-linked immunosorbent assay (ELISA). Bregs in spleens, cervical lymph nodes (LN), and periodontal tissues were detected by flow cytometry and immunofluorescence staining.

RESULTS: In the mouse model of periodontitis, IL-35 induced the expansion of CD1dhi CD5+ B10 cells with increased interleukin-10 (IL-10) and IL-35 production. IL-35 administration also attenuated alveolar bone loss and reduced the levels of pro-inflammatory cytokines in situ.

CONCLUSIONS: Following ligature-induced periodontitis in mice, IL-35 inhibited periodontal inflammation and alveolar bone resorption at least partially through the induction of B10 cells and IL-35+ Bregs. This article is protected by copyright. All rights reserved.