Immunotherapy represented by PD-1/PD-L1 and CTLA-4 has shown promising clinical effects in the treatment of tumors such as melanoma and non-small cell lung cancer, suggesting that it has great potential in the treatment of glioma. However, its clinical effect in glioma is limited due to tumor immune privilege which was induced by the glioma immunosuppressive microenvironment. Glioma cells can recruit a variety of cells, including immune cells, which move into niches by secreting cytokines and modifying these cells to a tumor-friendly phenotype. The rebellious immune cells may act as a wall to prevent non-tumor-friendly infiltration and may secrete cytokines to assimilate later recruited immune cells as friendly phenotype. Increasing evidence suggests that metabolic reprogramming (including in glioma and immune cells) is important in the dynamic progression of the immunosuppressive microenvironment.
Tumor cells undergo metabolic reprogramming in order to proliferate, resulting in a harsh microenvironment with acidity, nutrient deprivation, and hypoxia, while immune cells decline or die due to their inability to adapt. Immune cells can also be tamed or tricked by the cytokines and markers found in gliomas. All of these conditions cause a relative lack of functional immune cells, a condition known as immune cell exhaustion, in which case gliomas can continue to grow and become more malignant. However, the crosstalk between metabolic reprogramming and the immunosuppressive microenvironment remains limited and controversial, and a better understanding of them will provide novel solutions to glioma immunotherapy resistance and provide new insights into glioma therapy. Within this research theme, we welcome contributions related to the crosstalk between metabolic reprogramming and immunosuppressive microenvironment in glioma, from underlying molecular and cellular pathophysiology to clinical translation. Contents may include but are not limited to the following:
1) Glioma and immune cell metabolic reprogramming induced by nutrient deprivation, hypoxia, etc.
2) The role of glioma cell death (including ferroptosis, copper death, etc.) in the glioma immunosuppressive microenvironment.
3) Mechanisms underlying the induction of immune privilege by metabolic reprogramming in glioma/immune cells.
4) Mechanisms underlying immune cell exhaustion.
5) Recruitment and drainage of immune cells in gliomas and/or the central nervous system (CNS).
6) Translational therapeutic targets of metabolic reprogramming/immunity in glioma.
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
Immunotherapy represented by PD-1/PD-L1 and CTLA-4 has shown promising clinical effects in the treatment of tumors such as melanoma and non-small cell lung cancer, suggesting that it has great potential in the treatment of glioma. However, its clinical effect in glioma is limited due to tumor immune privilege which was induced by the glioma immunosuppressive microenvironment. Glioma cells can recruit a variety of cells, including immune cells, which move into niches by secreting cytokines and modifying these cells to a tumor-friendly phenotype. The rebellious immune cells may act as a wall to prevent non-tumor-friendly infiltration and may secrete cytokines to assimilate later recruited immune cells as friendly phenotype. Increasing evidence suggests that metabolic reprogramming (including in glioma and immune cells) is important in the dynamic progression of the immunosuppressive microenvironment.
Tumor cells undergo metabolic reprogramming in order to proliferate, resulting in a harsh microenvironment with acidity, nutrient deprivation, and hypoxia, while immune cells decline or die due to their inability to adapt. Immune cells can also be tamed or tricked by the cytokines and markers found in gliomas. All of these conditions cause a relative lack of functional immune cells, a condition known as immune cell exhaustion, in which case gliomas can continue to grow and become more malignant. However, the crosstalk between metabolic reprogramming and the immunosuppressive microenvironment remains limited and controversial, and a better understanding of them will provide novel solutions to glioma immunotherapy resistance and provide new insights into glioma therapy. Within this research theme, we welcome contributions related to the crosstalk between metabolic reprogramming and immunosuppressive microenvironment in glioma, from underlying molecular and cellular pathophysiology to clinical translation. Contents may include but are not limited to the following:
1) Glioma and immune cell metabolic reprogramming induced by nutrient deprivation, hypoxia, etc.
2) The role of glioma cell death (including ferroptosis, copper death, etc.) in the glioma immunosuppressive microenvironment.
3) Mechanisms underlying the induction of immune privilege by metabolic reprogramming in glioma/immune cells.
4) Mechanisms underlying immune cell exhaustion.
5) Recruitment and drainage of immune cells in gliomas and/or the central nervous system (CNS).
6) Translational therapeutic targets of metabolic reprogramming/immunity in glioma.
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.