Skip to main content
. 2020 Jun 2;23(6):314–318. doi: 10.1016/j.cjtee.2020.05.009

Table 1.

Part of immune cells involved in bone metabolism.

Cell type Cytokine Bone metabolism target References
Th1 cell IFN-γ, IL-2, TNF-α, and GM-CSF Inhibit osteoclast formation (IFN-γ degrades TRAF6) 36
Th2 cell IL-4, IL-5, IL-10, and IL-13 Inhibit osteoclast formation (IL-4, IL-5, and IL-13). Maintain anabolic activity of osteoblasts (promote the synthesis of PTH). 37,38
Th9 cell IL-9 Promote osteoclastogenesis (synergistically induces differentiation of CD4 + T cells into Th17 cells with TGF-β). 39
Th17 cell IL-17A, IL-17F, IL-21, and IL-22 Promote osteoclastogenesis (IL-17 promotes effector cell expression of RANKL). Inhibit osteoblast formation (IL-17 inhibits BMP-2 induced osteoblast differentiation). Promote bone resorption (IL-22 promotes the absorption activity of osteoclasts). 40, 41, 42
Treg cell CTLA- 4, IL-10 Inhibit osteoclast formation (CTLA-4 inhibits the production of RANKL and M-CSF). Inhibit osteoclast formation (IL-10 selectively inhibits calcium signaling downstream of RANK by inhibiting TREM-2 transcription). 43
NKT cell IL-15, TNF-α, and IFN-γ Recruiting monocytes (Upregulation of chemokine receptor and adhesion molecule expression). Promote osteoclastogenesis (IL-15 and RANKL synergistically induce osteoclastogenesis). Bidirectional regulation of osteoclast differentiation (TNF-α, IFN-γ). 44,45
γδT cell IL-6, IFN-γ Activate γδT cells to affect the regulation of osteoclastogenesis (IL-6 produces a promoting effect. IFN-γ production inhibition). 8

TRAF6: TNF receptor-associated factor 6, PTH: parathyroid hormone, RANKL: receptor activator of nuclear factor-κB ligand, CTLA- 4: CD80/cytotoxic T-lymphocyte associated protein 4, NKT: natural killer T.