Table 2.

Summary of the effects of Exos on host cells

No	Source of Exos	Biological activity	References
Neutrophil
1	MSCs	Have protective effects on neutrophil function and lifespan	[56]
2	MSCs	Reduce terminal complement activation complex C5b-9 to inhibit neutrophils accumulation	[57]
3	ADSCs	Decrease neutrophils apoptosis and increased their phagocytosis capacity	[58]
4	LPS-treated macrophages	Induce cytokine production and neutrophil migration	[59]
Macrophage
1	DPSCs	Facilitate macrophages to convert from M1 phenotype to M2 phenotype	[47]
2	TNF-α induced GMSCs	Induce anti-inflammatory M2 macrophage polarization	[50]
3	MSCs	Modify the polarization of M1 macrophages to M2 macrophages via shuttling miR-182	[60]
4	BMSCs	Increase M2 macrophage polarization	[61]
5	BMSCs	Inhibit M1 polarization and promotes M2 polarization in a murine alveolar macrophage cell line by inhibiting cellular glycolysis	[62]
6	FNDC5 pre-conditioned BMSCs	Play anti-inflammation effects and promote M2 macrophage polarization via NF-κB signaling pathway and Nrf2/HO-1 axis	[63]
7	hUCMSCs	Facilitate CD163 + M2 macrophage polarization, reduced inflammation, and increases anti-inflammatory responses	[64]
8	hUCMSCs	Inhibit M1 polarization and promoted M2 polarization through tumor necrosis factor receptor-associated factor 1 (TRAF1)	[65]
9	ADSCs	Upregulate mRNA expression of M2 macrophages	[66]
10	ADSCs	Induce anti-inflammatory M2 phenotypes through the transactivation of arginase-1 by Exo-carried active STAT3	[67]
11	ADSCs	Polarize macrophage to an anti-inflammatory phenotype via regulating the Nrf2/HO-1 expression	[68]
12	GMSCs	Facilitate macrophages to convert from M1 phenotype to M2 phenotype	[69]
Dendritic cell
1	MSCs	Decrease DC surface marker expression and modulates DC-induced immune responses	[70]
2	hUCMSCs	Suppress maturation and activation of DCs, and decreases the expression level of IL-23	[71]
3	regDCs	Suppress maturation of recipient DCs resulting in inhibition of bone resorptive cytokines	[72]
4	LECs	Promote the directional migratory in a CX3CL1/fractalkine-dependent fashion	[73]
T lymphocyte
1	MSCs	Increase Treg cell populations, inhibit T lymphocyte proliferation in a dose-dependent manner and decreases the percentage of CD4 + and CD8 + T cell subsets	[74]
2	MSCs	Upregulate IL-10 and TGF-β1 to promote proliferation and immune-suppression capacity of Tregs	[75]
3	MSCs	Inhibit the differentiation of Th2 cells via the regulation of the miR-146a-5p/SERPINB2 pathway	[76]
4	PDLSCs	Alleviate inflammatory microenvironment and keep Th17/Treg balance via Th17/Treg/miR‐155‐5p/SIRT1 regulatory network	[77]
5	CD137-modified ECs	Promote Th17 cell differentiation via NF-КB pathway mediated IL-6 expression	[78]
B lymphocyte
1	MSCs	Upregulate Breg-like cells in lymph nodes	[74]
Osteoclast
1	TNF-α-preconditioned GMSCs	Inhibit osteoclastogenic activity via exosomal miR-1260b to target Wnt5a-mediated RANKL pathway and	[50]
2	regDC	Result in inhibition of bone resorptive cytokines and reduces in osteoclastic bone loss	[72]
3	CMS-treated BMSCs	Impair osteoclast differentiation via inhibiting the RANKL-induced nuclear factor kappa-B (NF-κB) signaling pathway	[79]
4	ADSCs	Suppress NLRP3 inflammasome activation in osteoclasts and reduces bone resorption and recover bone loss	[80]
5	ADSCs	Antagonize osteocyte-mediated osteoclastogenesis	[81]
6	ADSCs	Inhibit pro-inflammatory cytokines production in high glucose-treated osteoclasts and restrains bone resorption	[82]
7	osteoblast	Inhibit the osteoclast differentiation via miR-503-3p/Hpse axis	[83]
8	EPCs	Promote bone repair by enhancing recruitment and differentiation of osteoclast precursors through LncRNA-MALAT1	(84)