期刊
JOURNAL OF CLINICAL PERIODONTOLOGY
卷 39, 期 12, 页码 1174-1182出版社
WILEY-BLACKWELL
DOI: 10.1111/jcpe.12009
关键词
dysfunction; immunomodulation; immunosuppression; inflammation; interleukin-10; interleukin-17; mesenchymal stem cells; periodontal ligament; regulatory T cells; Th17
资金
- National Key Basic Research Program of China [2007CB947304, 2010CB944801]
- Funding Project for Academic Human Resources Development in Institutions of Higher Learning Under the Jurisdiction of Beijing Municipality [PHR20090510]
- Funding Project to Science Facility in Institutions of Higher Learning Under the jurisdiction of Beijing Municipality [PXM 2009-014226-074691, PXM2011-014226-07-000066]
Aim The purpose of this study was to investigate the immunomodulatory properties of periodontal ligament stem cells derived from inflamed periodontal ligament tissues. Material and Methods Periodontal ligament stem cells were identified and isolated from healthy or inflamed periodontal ligament tissues. Peripheral blood mononuclear cells were cocultured with inflamed or healthy periodontal ligament stem cells, and T-lymphocyte proliferation was determined by incubation with carboxyfluorescein succinimidyl ester. T-helper cells (Th1/Th2, Th17) and regulatory T cells were analysed by flow cytometry. Cytokine profiles in supernatants were tested with a cytometric bead array. Results Compared to healthy cells, inflamed periodontal ligament stem cells showed significantly diminished inhibition of T-cell proliferation. In cocultures, stimulated peripheral blood mononuclear cells showed significantly less induction of CD4+CD25+FOXP3+ regulatory T cells and IL-10 secretion in the presence of inflamed compared with healthy periodontal ligament stem cells. Furthermore, suppression of Th17 differentiation and IL-17 production by inflamed periodontal ligament stem cells was significantly lesser than by healthy cells. Conclusion This study demonstrated that inflamed periodontal ligament stem cells had markedly dysfunctional immunomodulatory properties; this may contribute to an imbalanced immune response, acceleration of osteoclastogenesis and inflammatory alveolar bone loss in periodontitis.
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