Figure 5

Donor-derived MDSCs prolong allogeneic cardiac graft survival in a donor-specific manner. (A) Schematic diagram of the experimental design. C57BL/6 mice received a single-dose intravenous injection of 1 × 10⁶ BALB/c or C3H MDSCs. Cardiac grafts from C3H or BALB/c mice were transplanted into pre-sensitized C57BL/6 recipients. (B) Kaplan–Meier cumulative survival of allograft showing that the BALB/c MDSCs administration successfully prolong BALB/c allograft survival but fail to prolong C3H allograft survival, while C3H MDSCs administration prolong C3H allograft survival but fail to prolong BALB/c allograft survival. *p < 0.05, **p < 0.01, ***p < 0.001, log-rank test. (C) Schematic illustration of the experimental design to study the ex vivo donor-specific immunosuppressive function of donor MDSCs induced endogenous MDSCs (CD11b⁺Gr1⁺). Naïve C57BL/6 spleen T cells were labeled with CellTrace violet and were stimulated with BALB/c cDCs or C3H cDCs (third-party). CD11b⁺Gr1⁺ cells were isolated by FACS from BALB/c MDSCs treated C57BL/6 recipient splenocytes at POD7 (n = 3–4 per group) and were added as modulator. (D) CD4⁺ and CD8⁺ T cell proliferation in response to primary donor-type BALB/c cDCs or third-party C3H cDCs was analyzed by CellTrace violet dye dilution. Graphs showed the attenuated suppression efficiency (SE) of CD11b⁺Gr1⁺ cells in third-party compared to donor-type allo MLR setting. \(SE = \frac{{p\left( {w/oMDSC} \right) - p\left( {MDSC} \right)}}{{p\left( {w/oMDSC} \right)}} \times 100\%\). Mean ± SEM, *p < 0.05, **p < 0.01, two-tailed unpaired t test. Data represents one of 3 separate experiments.