4.2 Article

Dental pulp stem cells suppress the proliferation of lymphocytes via transforming growth factor-β1

期刊

HUMAN CELL
卷 28, 期 2, 页码 81-90

出版社

SPRINGER JAPAN KK
DOI: 10.1007/s13577-014-0106-y

关键词

Dental pulp stem cells; Immunogenicity; Immunosuppression; Regulatory T cells; Regenerative medicine

资金

  1. National Natural Science Foundation of China [81070799, 81222011]
  2. Excellent Young Researchers Foundation of Shandong Province [BS2010SW033]
  3. Science and Technology Activities of Beijing Overseas Students Preferred Foundation

向作者/读者索取更多资源

Dental pulp stem cells (DPSCs) possess self-renewal capability, multi-lineage differentiation potential, and can generate a dentin-pulp-like tissue in vivo, which is promising for tooth regeneration. To enlarge the cells resource of DPSCs and explore the feasibility of DPSCs-mediated immune therapy, it is prerequisite to investigate the immunological properties of DPSCs and the underlying mechanisms. Human DPSCs and peripheral blood mononuclear cells were isolated and cultured. Then we used lymphocytes proliferation assays, cytokines detection, Transwell cultures, neutralization experiments, and flow cytometry to examine the in vitro immune characteristics of DPSCs. We found that DPSCs failed to stimulate allogeneic T cells proliferation and suppressed T cells proliferation, B cells proliferation, and mixed lymphocyte reaction. In addition, DPSCs could up-regulate IL-10, down-regulate the production of IL-2, IL-17, and IFN-gamma, and did not affect the production of IL-6. Monoclonal antibody against transforming growth factor-beta 1 restored the T cells proliferation inhibited by DPSCs. Moreover, the population of regulatory T cells increased significantly and T-helper 17 cells decreased significantly in peripheral blood mononuclear cells co-cultured with DPSCs. These data confirmed that DPSCs are low immunogenic, could inhibit the proliferation of lymphocytes, regulate the production of cytokines in vitro, and the secretion of transforming growth factor-beta 1 may be involved in this event.

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