Figure 1
Figure 1. MSCIFNγR1− and MSCwt inhibit proliferation of PBMCs to a similar extent. (A) Proliferation of HLA-mismatched PBMCs in the absence (■) or presence (▩) of MSCwt; representative result of 5 independent experiments. MSCs inhibited PBMC proliferation in a dose-dependent manner. (B) PBMCs were inhibited by MSCs with IFNγR1 defect to a similar extent as by MSCwt (representative of n = 5). (C) Proliferation of HLA-mismatched PBMCs in the absence (■) or presence (▨) of MSCwt, when human rIFNγ was added to the cultures. PBMCs cocultured with MSCwt proliferated more vigorously in presence of rhIFNγ (representative of n = 5). (D) This effect mediated by rhIFNγ was even stronger when PBMCs were cocultured with MSCIFNγR1− (representative of n = 3). Data are shown as means of triplicates plus or minus standard deviation (±SD) of one representative experiment.

MSCIFNγR1− and MSCwt inhibit proliferation of PBMCs to a similar extent. (A) Proliferation of HLA-mismatched PBMCs in the absence (■) or presence (▩) of MSCwt; representative result of 5 independent experiments. MSCs inhibited PBMC proliferation in a dose-dependent manner. (B) PBMCs were inhibited by MSCs with IFNγR1 defect to a similar extent as by MSCwt (representative of n = 5). (C) Proliferation of HLA-mismatched PBMCs in the absence (■) or presence (▨) of MSCwt, when human rIFNγ was added to the cultures. PBMCs cocultured with MSCwt proliferated more vigorously in presence of rhIFNγ (representative of n = 5). (D) This effect mediated by rhIFNγ was even stronger when PBMCs were cocultured with MSCIFNγR1− (representative of n = 3). Data are shown as means of triplicates plus or minus standard deviation (±SD) of one representative experiment.

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