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(B) Inhibition of mouse liver MDSCs on T cell proliferation.
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Furthermore, as shown in Fig. 3C, the transferred BM-MDSCs significantly increased the frequency of CD11b+Gr-1+ MDSCs in mouse liver.
(C) Analysis of CD11b+Ly6G-Ly6Chigh CD11b+Ly6G-Ly6Chigh CD11b+Ly6G+Ly6Clow granulocytic monocyticMDSCs Conandreated mouse liver.
These results implicate that MDSC can protect mouse liver from ConA-mediated injury in a Treg-independent manner.
(A) Analysis of CD11b+ cells, CD11b+ Gr-1 cells, and CD11b+ Gr-1+ MDSCs in ConA-treated mouse liver and spleen.
(B) Analysis of the percentages of GFP-labeled BM-MDSCs in ConA-treated mouse liver, spleen, blood, and BM.
As shown in Fig. 2B, MDSCs purified from ConA-treated mouse liver strongly suppressed T cell proliferation.
(C) Frequencies of MDSCs and CD4+ CD69+ T cells in mouse liver.
To determine whether MDSCs inhibit T cell proliferation through ROS, we used DPI as ROS inhibitor and found that DPI could significantly inhibit the function of MDSCs isolated from the ConA-treated mouse liver (Fig. 2E).
(D) The inhibition of T cell proliferation by MDSCs isolated from mouse livers that were treated with or without DEX.
(D) Protein level of Arginase-1 were detected in MDSCs of ConA-induced mice liver.
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