English: Figure 1. Treg promote tissue repair and regeneration by modulating inflammation. Treg have demonstrated the ability to promote tissue repair and regeneration by controlling both the innate and adaptive immune systems. Following tissue injury, a cascade of immune events is triggered (steps 1–6) until a new tissue is formed (steps 7–8). Treg are involved in all these different steps. At the onset of inflammation, Treg can neutralize inflammatory cytokine secretion (e.g., IL-6, IFN-γ, TNF-α, and IL-1β) by inhibiting neutrophil extravasation via IL-10. In addition, Treg are able to promote apoptosis of neutrophils and encourage phagocytosis of dead neutrophils by macrophages. Concomitantly, Treg further inhibit monocyte activity, survival, and stimulate macrophage polarization toward an anti-inflammatory phenotype (M2) via the release of anti-inflammatory cytokines (e.g., IL-4, IL-10, IL-13). Similarly, Treg have the natural ability to suppress CD4 and CD8 T cell-mediated inflammation (via IL-10, TGF-β, and IL-35). Overall, these Treg-mediated mechanisms result in the inhibition of neutrophil, inflammatory macrophage, as well as CD4 and CD8 T-cell activity, which is generally favorable for tissue repair and regeneration. Dashed lines indicate a hypothetical mechanism. Red arrows indicate induction, while blue arrows indicate inhibition.