To utilize cancer immunotherapy effectively, it is important to understand the critical function of immune responses and metabolism in the tumor microenvironment. T cells are an important population of immune cells in the tumor environment that fight cancer cells. Recent findings have shown that the function and metabolites of cancer cells can lead to T cell dysfunction and the inhibition of T cell activation. For example, L-lactate production from cancer cells helps the suppressive ability of Tregs (eg. increased PD-1 expression) in the tumor microenvironment, which indicates that immune checkpoint inhibitor anti-PD-1 increases Tregs in the tumor microenvironment and prevents anti-tumor immunity. Fatty acid and cholesterol from tumor cells inhibit cytotoxicity by effector T cells (eg. increased exhausted T cells). Additionally, the conversion of tryptophan to kynurenine in tumor cells suppresses anti-tumor immunity by enhancing the generation and suppressive function of Tregs. Understanding the crosstalk between metabolism and T cell biology in the tumor environment can provide a new perspective on T cell based immunotherapies and improve quality of cancer treatment. In this collection, we would like to explore the modulations of T cell function and metabolism in the tumor microenvironment.
In this Research Topic, we would like to invite manuscripts related to tumor metabolites and T cell based anti-tumor immunity. We welcome Review/Mini-review, Original Research, Brief Research Report, Perspective, General Commentary, and Opinion articles, focusing on but not limited to:
1) Tumor metabolites control of T cell-based anti-tumor immunity
2) The role of anti-tumor chemicals in tumor metabolism and T cell based anti-tumor immunity
3) Immune checkpoint inhibitors (eg. anti-PD-1, anti-CTLA-4) and tumor metabolites
4) Insights into tumor metabolisms and T cell based anti-tumor immunity in cold and hot tumor conversion
5) Metabolic reprograming of tumor and T cell based anti-tumor immunity
6) Tumor metabolites and CAR-T therapy
To utilize cancer immunotherapy effectively, it is important to understand the critical function of immune responses and metabolism in the tumor microenvironment. T cells are an important population of immune cells in the tumor environment that fight cancer cells. Recent findings have shown that the function and metabolites of cancer cells can lead to T cell dysfunction and the inhibition of T cell activation. For example, L-lactate production from cancer cells helps the suppressive ability of Tregs (eg. increased PD-1 expression) in the tumor microenvironment, which indicates that immune checkpoint inhibitor anti-PD-1 increases Tregs in the tumor microenvironment and prevents anti-tumor immunity. Fatty acid and cholesterol from tumor cells inhibit cytotoxicity by effector T cells (eg. increased exhausted T cells). Additionally, the conversion of tryptophan to kynurenine in tumor cells suppresses anti-tumor immunity by enhancing the generation and suppressive function of Tregs. Understanding the crosstalk between metabolism and T cell biology in the tumor environment can provide a new perspective on T cell based immunotherapies and improve quality of cancer treatment. In this collection, we would like to explore the modulations of T cell function and metabolism in the tumor microenvironment.
In this Research Topic, we would like to invite manuscripts related to tumor metabolites and T cell based anti-tumor immunity. We welcome Review/Mini-review, Original Research, Brief Research Report, Perspective, General Commentary, and Opinion articles, focusing on but not limited to:
1) Tumor metabolites control of T cell-based anti-tumor immunity
2) The role of anti-tumor chemicals in tumor metabolism and T cell based anti-tumor immunity
3) Immune checkpoint inhibitors (eg. anti-PD-1, anti-CTLA-4) and tumor metabolites
4) Insights into tumor metabolisms and T cell based anti-tumor immunity in cold and hot tumor conversion
5) Metabolic reprograming of tumor and T cell based anti-tumor immunity
6) Tumor metabolites and CAR-T therapy