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An expanding body of literature has described the roles of extracellular vesicles (including exosomes) in both tumor progression and suppression (1, 2). A recent report by Poggio et al. contributes to this discussion by revealing that exosomes bearing the immune checkpoint protein PD-L1 promote tumor progression by compromising T cell activity (3). The authors used various tumor cell lines and genetic approaches in the context of a mouse in vivo system to show that disrupting either PD-L1 expression or exosome biogenesis supported anti-tumor immunity. In addition, their data reinforces the notion that anti-PD-L1 immunotherapy is less active against PD-L1-carrying exosomes, suggesting that regimens could potentially be made more effective by the inclusion of agents specifically targeting exosomes and exosomal PD-L1. Finally, the authors found that blocking exosome generation at one tumor site gives rise to systemic immune activation against other remote tumor challenges.
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