Table 5.

Mechanism of action with MSCs and EVs on macrophage.

Cell type	Immune cell	Mechanism	Effect	Reference
MSC	macrophage	Through TGF-β/Akt/FoxO1 pathway	toward M2 phenotype polarization	(112)
UC-MSC	macrophage	regulating macrophage metabolic pathways	affect M1/M2 balance	(113)
MSC-Exo	macrophage	down-regulating IL-23 and IL-22	enhances the anti-inflammatory phenotype of macrophages, promoting inflammation remission	(114)
AD-MSCs	macrophage	–	toward M2 phenotype polarization	(115)
MSC-Exo	macrophage	through miR-223/pKNOX1 pathway	promoting macrophages differentiation toward M2	(116)
MSC-EVs	macrophage	through TLR4/NF-κB/PI3K/Akt signaling cascade	toward M2 phenotype polarization	(117)
UC-MSC/exosomes	macrophage	increased the proportion of M2 macrophage polarization	attenuate diffuse alveolar hemorrhage (DAH) induced inflammatory responses and alveolar hemorrhage	(118, 119)

MSC, Mesenchymal stem cells; MSC, Mesenchymal stem cells; MSC-EVs, MSC derived Extracellular Vesicles; MSC-exo, MSC derived Exsome; UC-MSC, umbilical cord Mesenchymal stem cells; AD-MSC, adipose MSC; TRAF6, IR7; IL-10, interleukin 10; IL-23, interleukin 23 ;IL-22 , interleukin 22; pKNOX1, PBX/knotted 1 homeobox 1; NF-KB, nuclear transcription factor-kappa B; PI3K, phosphoinositide 3-kinase; PGE2, Prostaglandin E2; TLR4, Toll-like Receptor 4; DAH, diffuse alveolar hemorrhage.