Involvement of Cathepsins in Innate and Adaptive Immune Responses in Periodontitis

Figure 1

A schematic illustration of the cathepsin-related immune responses in periodontitis linking to the diseases within the whole body. In the bacteria (components)-stimulated cells, cathepsin B involves in activation of TLR signaling to produce IL-1β, TNF-α, and amyloid (A) β, and cathepsin S involves in maturation of MHC class II for driving CD4⁺ (helper) T cells to produce IFN-γ (Th1) and IL-17 (Th17). Cathepsin K involves in activation of the TLR/autophagy pathway to produce type I interferon (IFN). The periodontitis cathepsin-related proinflammatory mediators involve in systemic diseases and Alzheimer’s disease via the circulation.