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. 2016 Jan 14;113(5):E587–E596. doi: 10.1073/pnas.1518130113

Fig. 1.

Fig. 1.

Exosomes released by latent EBV-infected LCLs trigger antiviral immunity in DCs. (A) Schematic representation of experimental design: primary DCs were incubated with exosomes derived from EBV+ LCLs or EBV− control B cells (BJAB), and a gene-expression profile was performed using high-density arrays after 18 h of incubation. (B and C) GO analysis performed with DAVID showing the top modulated pathways in DCs exposed to EBV− control B-cell (B) and EBV+ LCL (C) exosomes compared with untreated DCs. (D) Fold-difference of IFN-stimulated genes in DCs exposed to LCL exosomes compared with control exosomes. (E) Schematic representation of a transwell coculture system: exosome-producing B cells (upper compartment) and recipient DCs (lower compartment) are separated by a 1-µm pore size membrane, which allows the passage of exosomes. (F) Quantitative PCR (qPCR) for IFITM1 and IFITM3 in DCs at indicated time points during coculture using a transwell with either 1- or 0.4-µm membrane pores. Transcript levels are normalized to GAPDH and expressed as fold-increase relative to t = 0.