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. 2018 Mar 7;4(3):eaar2766. doi: 10.1126/sciadv.aar2766

Fig. 1. Glioblastoma EVs inhibit T cell activation in an antigen-specific manner.

Fig. 1

(A) EVs from human GSC cultures inhibit both CD4+ and CD8+ T cell activation and proliferation. PBMCs (isolated from eight human volunteers, n = 8) were treated with anti-CD3 (500 ng/ml) to activate TCR signaling in the presence or absence of GSC EVs (5 μg/ml; isolated from four different GSCs, that is, n = 4) for 2 days. Top: Dot plots of CD69 and CD25 and proliferation flow cytometry data. Bottom: Percent changes of CD69 (left) and CD25 (middle) compared to anti-CD3 alone and percent change of proliferating cells (right) compared to anti-CD3 treatment alone after 3 days for CD4+ and CD8+ T cells, measured by carboxyfluorescein diacetate succinimidyl ester (CFSE) content. (B) EVs from CT2A glioma cells inhibited CD8+ T cells in an antigen-specific manner. Percent CD69 expression change (left) of CD8+ T cells isolated from transgenic P14 mice reacting against gp33 peptide presented by DC ± CT2A EVs; proliferation change (right) of gp33 antigen–specific P14 CD8+ T cells ± CT2A EVs measured by CFSE (n = 4). Statistical analysis was performed by two-tailed Student’s t test (****P < 0.0001). Bars represent means ± SD of each of the eight T cell preparations after incubation with one EV preparation from each of the four gender-matched GSC EVs.