Abstract
Glioblastoma Multiforme (GBM) is the most common and aggressive form of intracranial tumors with poor prognosis. In recent years, tumor immunotherapy has been an attractive strategy for a variety of tumors. Currently, most immunotherapies take advantage of the adaptive anti-tumor immunity, such as cytotoxic T cells. However, the predominant accumulation of tumor-associated microglia/macrophages (TAMs) results in limited success of these strategies in the glioblastoma. To improve the immunotherapeutic efficacy for GBM, it is detrimental to understand the role of TAM in glioblastoma immunosuppressive microenvironment. In this review, we will discuss the roles of CD47-SIRPα axis in TAMs infiltration and activities and the promising effects of targeting this axis on the activation of both innate and adaptive antitumor immunity in glioblastoma.
Highlights
Glioblastoma (GBM) is the most common primary malignant brain tumor in adults and is characterized by invasive growth and frequent recurrence
Accumulating evidence suggests that the GBM microenvironment is characterized by high myeloid cell content, relatively few tumor-infiltrating lymphocytes (TILs) [7, 8]and T cell dysfunction [9]
NI-1801 destroy mesothelin-positive solid tumors through the innate immune system; VEGFR1D2-SIRPaD1 consists of the second extracellular domain of VEGFR1 (VEGFR1D2) and the first extracellular domain of SIRPa (SIRPaD1), which exerted potent anti-tumor effects via suppressing VEGF-induced angiogenesis and activating macrophage-mediated phagocytosis [68,69,70]
Summary
Glioblastoma (GBM) is the most common primary malignant brain tumor in adults and is characterized by invasive growth and frequent recurrence. Targeting the immune checkpoint complex CD47-SIRPa has been shown as a promising anti-tumor strategy that may remodel the GBM microenvironment, restore innate and adaptive immunity functions, and improve the prognosis of patients with GBM. These promising strategies still need considerable refinement before becoming the standard clinical treatment options for GBM. NI-1801 destroy mesothelin-positive solid tumors through the innate immune system; VEGFR1D2-SIRPaD1 consists of the second extracellular domain of VEGFR1 (VEGFR1D2) and the first extracellular domain of SIRPa (SIRPaD1), which exerted potent anti-tumor effects via suppressing VEGF-induced angiogenesis and activating macrophage-mediated phagocytosis [68,69,70]. Among the immunological checkpoint inhibitors, Hu5F9-G4, TTI-621, and TTI-622 are undergoing Phase I clinical trials, the complete data have not been published [71]
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