ArticleJournal of extracellular vesicles2026
NF1 Leucine Rich Domain-Derived Extracellular Vesicles Remodel the Glioblastoma Immune Microenvironment via an ADAM17-Associated Inflammatory Program.
Article in Journal of extracellular vesicles, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Extracellular vesicles (EVs) are increasingly recognized as mediators of intercellular communication in cancer. We previously demonstrated that re-expression of the leucine-rich domain (LRD) of neurofibromin (NF1) suppresses glioblastoma (GBM) invasion and limits microglia/macrophage infiltration into the tumor microenvironment (TME). Given the central role of tumor-associated microglia/macrophages (TAMs) in GBM progression, we investigated whether NF1-LRD-containing EVs (NF1-LRD-EVs) could modulate TAM function and remodel the TME. Our results showed that NF1-LRD-EVs attenuated microglia and macrophage recruitment in migration assays, consistent with reduced microglia/macrophage recruitment observed in vivo. In parallel, treatment with NF1-LRD-EVs enhanced phagocytic activity of both microglia and iPSC-derived macrophages, accompanied by induction of pro-inflammatory cytokines TNF-α, IL-6, and IL-1β, and downregulation of immunosuppressive mediators such as Arginase-1 and IL-10. Mechanistically, NF1-LRD-EVs induced ADAM17-associated inflammatory signaling, accompanied by NF-κB activation. Pharmacological inhibition of ADAM17 reduced TNF-α release and attenuated NF-κB activation, supporting a role for ADAM17-dependent signaling in amplifying this inflammatory response. Together, these findings show that NF1-LRD-EVs reprogram TAMs toward a pro-inflammatory phenotype and modulate the GBM immune microenvironment. These results provide a framework for understanding NF1-LRD-EV-mediated immune regulation and support further investigation of EV-mediated immune modulation of the TME.
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