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Table 2 Summary of the effects of Exos on host cells

From: Advances of exosomes in periodontitis treatment

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)