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. 2017 Feb 21:8:145.
doi: 10.3389/fimmu.2017.00145. eCollection 2017.

CD8+ T Cells in Chronic Periodontitis: Roles and Rules

Elsa M Cardoso  1 , Fernando A Arosa  1
Affiliations

CD8+ T Cells in Chronic Periodontitis: Roles and Rules

Elsa M Cardoso et al. Front Immunol. .
No abstract available

Keywords: CD8+ T cells; alveolar bone; cytokines; gingiva; periodontal disease; regulatory; suppressor; tissue repair.

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Figures

Figure 1
Figure 1
Proposed simplified model for the role of gingival CD8+ T cell-derived cytokines and factors in alveolar bone homeostasis in health and chronic periodontitis. (A) Anatomy of soft and hard periodontal tissues showing selected cells: CD8+ T cells, herein collectively referred as memory CD8+ T cells or TM (blue), osteoblasts (green), and osteoclasts (purple), in healthy periodontal tissues (left panel) and in chronic periodontitis (right panel). Note accumulation of pathogenic bacteria on the tooth surface, formation of a pocket with gingival crevicular fluid (GCF) accumulation, gingival attachment loss, inflamed gingiva (reddish), as well as loss of alveolar bone in chronic periodontitis due to imbalance in the equilibrium between osteoblastogenesis and osteoclastogenesis toward the latter (right panel). (B) Bone-protective versus bone-destructive factors that can be produced by gingival CD8+ TM cells. Under homeostatic conditions (left panel), IL-10 and TGF-β secreted by CD8+ TM cells suppress osteoclastogenesis, while Wntb10 promotes differentiation of mesenchymal stem cells (MSC) into osteoblasts and inhibits their apoptosis. In addition, CD8+ TM cells secrete amphiregulin (AREG) that downplays gingival inflammation and promotes epithelial and stromal tissue repair (data not shown, see text). Overall, these bone promoting cytokines counteract the bone loss induced by commensal bacteria (see text). The role of IFN-γ and IL-17 under homeostatic conditions on osteoclastogenesis and osteoblastogenesis is uncertain (dashed lines). Under chronic periodontitis (right panel) high levels of TNF-α, and perhaps of IFN-γ and IL-17, produced in response to pathogenic bacterial colonization surpass the protective role of the aforementioned cytokines, promoting osteoclastogenesis and increasing apoptosis of osteoblasts, thus favoring bone loss.
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