Table 2.
Sources of MSCs | Animal model | Route of administration | Dose | Main outcome | |
---|---|---|---|---|---|
Chen et al., 2022 (17) | Human UC-MSCs | Mouse model induced by IMQ cream | Intravenous/subcutaneous | 2 × 106 cells | Reducing the severity of psoriasis-like dermatitis. Delaying the appearance of skin lesions. Accelerating the recovery of skin lesions by reducing the number of Th1 and Th17 cells and their secreted pro-inflammatory products. Increasing the number of Treg cells. |
Chen et al., 2019 (64) | Human UC-MSCs | Mouse model induced by IMQ cream | Intravenous | 1 × 106 cells | Inhibiting the infiltration of immune cells into the dermal layer Suppressing the secretion of IFN-γ from pDCs |
Ye et al., 2022 (21) | Human gingiva-derived MSCs | Mouse model induced by IMQ cream | Intravenous | 2 × 106 cells on 1 and 4 days | Reducing pro-inflammatory cytokines including IFN-γ, TNF-α, IL-6, IL-17A, IL-21 secreted by Th1 and Th17 cells Promoting the number of Treg cells |
Sah et al., 2016 (65) | Human UC-MSCs (SOD3-tranduced) | Mouse model induced by IMQ cream | Subcutaneous | 2 × 106 cells | Ameliorating the symptoms of skin lesion by regulating the inflammatory pathways including TLR-7, NFκB, MAPK, and JAK-STAT pathways |
Meng et al., 2021 (66) | Human DPSCs (HGF-transduced) | Mouse model induced by IMQ cream | Intravenous | 2 × 106 cells | Ameliorating the psoriasis-like erythema, scaling, and thickening and the expression of CK6 and CK17. Decreasing inflammatory cytokines such as IFN-γ, IL-6, and TNF-α. Reducing the number of Th1. Increasing the number of Th2.i90op. |
Zhang et al., 2022 (67) | Human UC-MSCs (IFNγ-sEVs) |
Mouse model induced by IMQ cream | Intradermal | 150 µg | Reducing the symptom of psoriasis through decreasing the levels of pro-inflammatory cytokines including IL-17A, IFN-γ, IL-6, and TNF-α and Th17 cells. Increasing the population of Th2 cells in both spleen and skin. |
Zhang et al., 2022 (68) | Human UC-MSCs (EVs) | Mouse model induced by IMQ cream | Subcutaneous | 50 µg | Reducing proinflammatory cytokines and chemokines including IL-17, IL-23, TNFα, and CCL20 suppressing the activation of DCs through inhibiting the JAK-STAT pathway |