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Fig. 2 | Cell Communication and Signaling

Fig. 2

From: Acute myeloid leukemia-derived exosomes deliver miR-24-3p to hinder the T-cell immune response through DENN/MADD targeting in the NF-κB signaling pathways

Fig. 2

The expression level of miR-24-3p in CD3 T cells and EXOs in AML patients. Relative miR-24-3p expression assessed by qRT‒PCR (A) in EXOs isolated from peripheral blood AML blast culture supernatant (n = 10) compared to that of HDs (n = 3), (B) in HD-isolated CD3 T cells after incubation with AML EXOs (n = 8) or HD EXOs (n = 5), (C) and in CD3 T cells freshly isolated from AML patient peripheral blood (n = 16) compared to that of 10 HDs. DE HD CD3 T cells were cultured in the presence of miR-24-3p-enriched EXOs (Exo-miR-24-3p) or antimiR-24-3p-enriched EXOs (Exo-antimiR-24-3p) for 5 days; CD3 T cells cultured in the medium were used as controls. The degree of apoptosis was measured by FACS (cells were labeled with annexin-V-FITC and PI). Enriched EXOs (E-EXOs) were obtained from the culture supernatant of the K562 blast cell line overexpressing miR-24-3p after lentivirus-24-3p vector (miR-24-3p-EXO) transduction or anti-miR-24-3p-EXO in which anti-miR-24-3p was expressed by transducing K562 cells with a lenti-anti-miR-24-3p vector. D Treatment of T cells with E-EXOs increased miR-24-3p expression in T cells. E miR-24-3p-EXO treatment significantly increased the apoptosis level of T cells (***, p < 0.001), while anti-miR-24-3p-EXO significantly decreased apoptosis compared to the control (*** p < 0.002). Bar graphs represent the mean ± SEM *p < 0.05, **p < 0.01, ***p < 001

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