Figure 1.

Cellular and molecular mechanisms of GBM immunotherapy. GBM cells overexpress PDL1, CD47, and other immunosuppressive molecules and bind the ligands present on cytotoxic T lymphocytes (CTLs) and macrophage, and thereby inhibit the innate and adaptive immune function, leading to the immune escape of GBM. Targeting immune checkpoint molecules such as PDL1, CD47, and CTLA4 can activate both innate and adaptive anti-tumor immunity. The mechanism of oncolytic virus therapy is mainly via the creation of viruses that can selectively infect GBM cells, defeat GBM cells, and enhance adaptive anti-tumor immune responses by the dendritic cell and CTL. Several tumor-related antigens (e.g., IL-13Ra2, EGFRvIII) are expressed on the surface of GBM cells and are used as specific targets for (CAR) T cell therapy to achieve a precise treatment objective. The vaccination strategy mainly mediates the activation of CTLs by antigen-presenting cells, thus killing GBM cells.