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Updated: Jun 4, 2026

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Isolation, Processing and Analysis of Murine Gingival Cells
Published on: July 2, 2013
B10 Adoptive Transfer Ameliorates Inflammation and Bone Loss in Experimental Periodontitis Through Promoting
Guoqin Cao1,2, Elaheh Dalir Abdolahinia1, Takumi Memida1
1Department of Oral Science and Translational Research, College of Dental Medicine, Nova Southeastern University, 3200 South University Drive, Fort Lauderdale, FL, 33328, USA.
Inflammation
|June 3, 2026
Summary
Regulatory B cells (B10) transfer combats periodontal inflammation and bone loss by promoting pro-resolving macrophages. This interaction enhances neutrophil clearance and macrophage autophagy, crucial for resolving periodontitis.
Area of Science:
- Immunology
- Periodontology
- Inflammation Research
Background:
- Immune cell interactions regulate inflammatory responses.
- Interleukin-10 (IL-10)-expressing regulatory B cells (B10) secrete IL-10, potentially resolving periodontal inflammation.
- The dynamic interaction between B10 cells and macrophages in periodontitis requires further investigation.
Purpose of the Study:
- To investigate the dynamic infiltration of B10 cells and macrophages in experimental periodontitis.
- To elucidate B10-induced macrophage differentiation and pro-resolving functions in vivo.
- To determine the role of B10-macrophage interactions in mitigating periodontal disease progression.
Main Methods:
- Adoptive transfer of B10 cells into a mouse model of experimental periodontitis.
- Macrophage depletion using clodronate liposomes.
- In vivo imaging (IVIS), Micro-CT, TRAP staining, immunohistochemistry, immunofluorescence, and LC-MS/MS were employed to assess cellular infiltration, bone loss, cytokine production, efferocytosis, autophagy, and specialized pro-resolving mediators (SPMs).
Main Results:
- B10 adoptive transfer significantly inhibited alveolar bone resorption and osteoclast differentiation, while increasing pro-resolving macrophages.
- Gingival tissues showed elevated IL-10, Arg-1, YM-1, ATG5, LC3B, and CD68+Ly6G+ cells, alongside reduced IL-17A, TNF-α, and IL-1β.
- Macrophage depletion attenuated B10-mediated suppression of bone loss and certain inflammatory markers, but RvD2 release was macrophage-dependent.
Conclusions:
- B10 adoptive transfer effectively reduces inflammation and bone loss in experimental periodontitis.
- This therapeutic effect is mediated by inducing macrophage pro-resolving functions, including RvD2 production, enhanced neutrophil clearance, and autophagy.
- The B10-macrophage axis represents a promising therapeutic target for periodontitis.
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