Natural Killer T (NKT) Cells and Periodontitis: Potential Regulatory Role of NKT10 Cells

Figure 5

Role of NKT cells during periodontal health and disease. During periodontal health, the low-grade antigenic load of commensal microbial origin favors the differentiation and activity of NKT2 cells and eventually NKT10 cells. In this context, NKT2 and NKT10 cells could promote the transactivation of Th2 and Treg lymphocytes, which inhibit osteoclastogenesis and M1 macrophage activation, and induce osteoblastogenesis and M2 macrophage activation, thus favoring periodontal tissue homeostasis. During periodontitis, the host’s immune response is triggered against the dysbiotic bacterial communities colonizing the subgingival environment. During this process, the antigen-presenting cells present the microbial and tissue-damage antigens to the distinct immune effector cells; therefore, they can present antigens of a glycolipid nature to NKT cells. In this context, activated NKT cells acquire the potential to differentiate into NKT1 and NKT17 cells. Then, NKT1 and NKT17 cells could promote the transactivation of Th1 and Th17 lymphocytes, which induce the activation of M1 macrophages and the differentiation and function of osteoclasts, and consequently, promote periodontal inflammation and alveolar bone resorption. IFN, interferon; IL, interleukin; Treg, regulatory T lymphocytes; NKT, Natural Killer T cell; RANKL, receptor activator of nuclear factor κΒ ligand; TGF, transforming growth factor; TNF, necrosis factor tumors. (Created with http://BioRender.com).