Ewelina M. Bartoszek

Nov 8, 2024 | nature.com | Tomas Martins |Deniz Kaymak |Nazanin Tatari |Sabrina Hogan |Marie-Françoise Ritz |Ewelina M. Bartoszek | +9 more

AbstractA significant challenge for chimeric antigen receptor (CAR) T cell therapy against glioblastoma (GBM) is its immunosuppressive microenvironment, which is densely populated by protumoral glioma-associated microglia and macrophages (GAMs). Myeloid immune checkpoint therapy targeting the CD47-signal regulatory protein alpha (SIRPα) axis induces GAM phagocytic function, but CD47 blockade monotherapy is associated with toxicity and low bioavailability in solid tumors.