biostudies-literatureGao CNational Natural Science Foundation of ChinaTianjin Binhai New Area Health Commission Science-technology Innovation Plan Projects241https://www.ebi.ac.uk/biostudies/studies/S-EPMC7301524biostudies-literatureUnknown11(1)<h4>Background</h4>Mesenchymal stem cells (MSCs) have become a promising candidate for cell-based immune therapy for acute rejection (AR) after heart transplantation due to possessing immunomodulatory properties. In this study, we evaluated the efficacy of soluble fibronectin-like protein 2 (sFgl2) overexpressing mesenchymal stem cells (sFgl2-MSCs) in inhibiting AR of heart transplantation in mice by regulating immune tolerance through inducing M2 phenotype macrophage polarization.<h4>Methods and results</h4>The sFgl2, a novel immunomodulatory factor secreted by regulatory T cells, was transfected into MSCs to enhance their immunosuppressive functions. After being co-cultured for 72 h, the sFgl2-MSCs inhibited M1 polarization whereas promoted M2 of polarization macrophages through STAT1 anStem cell research & therapyMesenchymal stem cells transfected with sFgl2 inhibit the acute rejection of heart transplantation in mice by regulating macrophage activation.PMC73015242017BWKY03681570375Liu YLi ZChen MLu JQi FJia HLi PDu XWang XChang YZhang BGao CfalseMesenchymal stem cells transfected with sFgl2 inhibit the acute rejection of heart transplantation in mice by regulating macrophage activation.<h4>Background</h4>Mesenchymal stem cells (MSCs) have become a promising candidate for cell-based immune therapy for acute rejection (AR) after heart transplantation due to possessing immunomodulatory properties. In this study, we evaluated the efficacy of soluble fibronectin-like protein 2 (sFgl2) overexpressing mesenchymal stem cells (sFgl2-MSCs) in inhibiting AR of heart transplantation in mice by regulating immune tolerance through inducing M2 phenotype macrophage polarization.<h4>Methods and results</h4>The sFgl2, a novel immunomodulatory factor secreted by regulatory T cells, was transfected into MSCs to enhance their immunosuppressive functions. After being co-cultured for 72 h, the sFgl2-MSCs inhibited M1 polarization whereas promoted M2 of polarization macrophages through STAT1 an2020-01-01T00:00:00Z2020 Jun2025-04-21T21:09:47.445Z2020-06-25T07:31:39ZS-EPMC73015243255282310.1186/s13287-020-01752-1