CD25+ B cells produced IL‐35 and alleviated local inflammation during experimental periodontitis.

Background and objective: Host immunity is crucial during periodontal inflammations. B cells are considered to have a function of immunoregulation, and TLRs are considered to be crucial in this process. The present study illustrates the potential roles and rules of CD25+ B cells during periodontitis, especially its effect on regulating host IL‐35 level and Th1, Th17, and Treg differentiation. Material and methods: The proportion of local and systemic CD25+ B cell subpopulations from periodontitis models were identified by flow cytometry. To illustrate further mechanism, B cells were cultured with a different type of TLR activators. Expression of IL‐10, IL‐35, and TGF‐β was detected by ELISA and real‐time PCR. We also set adoptive transfer models by using CD25+ B cells. Alveolar bone erosion, proportion of Th1, Th17, and Tregs, and levels of IFN‐γ, TNF‐α, IL‐1β, and IL‐17 were identified. Result: Periodontitis induces more CD25+ B cell subpopulations and promotes their IL‐10, IL‐35, and TGF‐βproduction. TLR activators enhanced Breg proliferation and function. LPS+CpG obviously induced more CD25+ B cell differentiation and production of IL‐10, IL‐35, and TGF‐β. Adoptive transfer of CD25+ B cells reduces alveolar bone destruction and local Tregs, proportion, especially the local level of IFN‐γ and IL‐17. In addition, adoptive transfer of CD25+ B cells remedies the pathological change in the proportion of IL‐1β and Th1/Th17 in local lesions. We did not find any significant difference in peripheral blood, regardless of group and detected items. Conclusion: Results of the present study clarify that CD25+ B cells enlarged and produced more IL‐10, IL‐35 and TGF‐β during periodontitis, activation of TLR4 and TLR9 played crucial roles in this process. Also, CD25+ B cells alleviated periodontal inflammation and alveolar bone resorption. Our findings further expanded the potential of B cells during periodontitis. [ABSTRACT FROM AUTHOR]