Fig. 3

Roles of SUSD2⁺ eMSCs and MenSCs in immunity. A TGF-β promotes the differentiation of Tregs that inhibit T-lymphocyte proliferation. A83-01 increases the T-lymphocyte proliferation through the inhibition of the TGF-β signaling-dependent Treg differentiation, but SUSD2⁺ eMSCs continue to inhibit the lymphocyte proliferation via an uncertain mechanism independent of the TGF-β signaling from that of MSC from other tissues. B MenSCs inhibit the phenotypic differentiation of human peripheral blood monocytes into immature and mature DCs. MenSCs can also affect the proliferation of monocytes in a dose-dependent manner. In vivo studies, after the intravenous injection of MenSCs, the proportion of CD4⁺ and CD8⁺ T cells in spleen was significantly down-regulated and the percentage of CD4⁺CD25⁺Foxp3⁺ regulatory T cells (Treg) and Breg (CD19⁺IL‐10⁺) in spleen was significantly up-regulated. The serum levels of IL-1β, IL-6, and TNF-α in mice receiving MenSCs transplantation are lower, but the expression level of IL-10 is higher. CXCL12 secreted by MenSCs also increases the percentage of Treg, Breg, and M2 cells. MenSC-derived exosomes can resolve inflammation through the induction of the M1-M2 macrophages polarization. MenSCs treatment may inhibit the proliferation of B cells to reduce the production of IgM and IgG antibodies