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Ntal settings, systemically infused gingival MSCs homed to the wound web page, promoted host macrophage differentiation into M2, and enhanced wound repair [184]. In the models of acute lung injury, MSCs shifted macrophage phenotype from M1 to M2 attenuating lung tissue inflammation [185, 186]. In a single study, the effect was partially due to insulin-like growth element I (IGF-I) secreted by MSCs

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