Table 2 Summary of the effects of Exos on host cells

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)