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English: Figure 2. Treg likely promote tissue repair and regeneration in a tissue-specific manner. Treg play an important role in the repair and regeneration of skeletal muscle, heart muscle, skin and hair, lung, bone, and central nervous system (CNS). (A) In skeletal muscle, IL-33 participates to Treg recruitment into the site of injury. Treg inhibit M1 macrophage-mediated inflammation, which promote transition to the resolution phase. Treg also directly activate satellite cell proliferation and differentiation through Areg. (B) In the heart, Treg are recruited via CCR5 signaling (e.g., CCL3 and CCL4) allowing inhibition of Th1 cell activity and inhibition of M1 macrophages. (C) In skin and hair, mechanism of Treg recruitment is still unknown, but upon recruitment, Treg inhibit M1 macrophage inflammatory activity and promote wound closure and hair growth via the Jag1-Notch signaling pathway. (D) In the lung, Treg inhibit M1 macrophage inflammatory activity and encourage proliferation and differentiation of damaged alveolar type 2 epithelial cells (AECII) into AECIs. This step can be mediated by Areg or CD103 to E-cadherin ligand-receptor binding. Alternatively, Treg could potentially activate progenitor bronchioalveolar stem cells (BASCs) to differentiate into AECII cells. Concurrently, Treg prevent fibrosis by inhibiting fibrocyte recruitment and proliferation via CXCL12. (E) In the bone, Treg are most likely recruited via CCL22, which act on inhibiting Th1, CD8+, and M1 macrophages to support osteoblast progenitor differentiation. (F) In CNS, Treg are recruited by IL-33 and play a reparative role by encouraging M2 macrophage polarization to facilitate re-myelination and differentiation of oligodendrocytes. Treg may also directly act on oligodendrocytes via CCN3. Dashed lines indicate a hypothetical mechanism. Red arrows indicate induction, while blue arrows indicate inhibition.