Abstract

Glioblastoma (GBM) is a highly aggressive and heterogeneous tumor, with a strong immunosuppressive tumor microenvironment (TME), in which tumor-associated macrophages (TAM) play a crucial role. This immunosuppressive phenotype is detrimental to the efficacy of chimeric antigen receptor (CAR) T cell therapy. We believe that oncolytic adenoviruses can overcome some of the mechanisms involved in TME immunosuppression. Here, we investigate the capacity of the oncolytic adenovirus ICO15K to reprogram the GBM TME, with a special focus on promoting the transition from a pro-tumoral M2 to a pro-inflammatory M1 TAM phenotype.

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