Figure 2.
Role and mechanisms of MSCs/MSC-Evs in the regulation of AD.MSCs can regulate the immune system by releasing Evs and soluble cytokines. The secretion of IL-10 by MSCs inhibits dendritic cell proliferation and differentiation. PGE2 and TGF-β inhibit the proliferation, activation, and IgE production of Th17 cells and B cells while promoting the proliferation, maturation, and production of IL-10 by Tregs cells. Additionally, PGE2, TGF-β, EGF, has-miR-214-3p, has-miR-424-5p, and other intra-Evs miRNAs inhibit mast cell maturation and degranulation. VEGF, EGF, and HGF promote the proliferation of fibroblasts and vascular endothelial cells, while Evs miRNAs miR-125a-3p inhibit Th2 cell proliferation and activation. Moreover, miR-147a and miR-21-3p activate the PI3K/Akt pathway and inhibit MEF2A and VEGFA, promoting the proliferation of keratinocytes and vascular endothelial cells and ultimately facilitating the healing of skin lesions.
Abbreviations: Evs, Extracellular vesicles; CKs, cytokines; DCs, Dendritic cells; Th2 cells, T helper 2 cells; Th17 cells, T helper 17 cells; MCs:mast cells; Tregs cells: Regulatory T cells; VEGF, Vascular Endothelial Growth Factor; EGF, Epidermal Growth Factor; TGF-β1 Transforming growth factor-β; HGF, Hepatocyte Growth Factor; PGE2, Prostaglandin 2; MIP-2, macrophage inflammatory protein 2; IL-4, interleukin 4; IL-10, interleukin 10; IL-13, interleukin 13; IL-17A, interleukin 17A; PI3K/Akt, Phosphatidylinositol 3-kinase protein kinase b pathway; NF-κB, NF-κB signaling pathway; JAK/STAT, JAK/STAT signaling pathway.
