Nowadays, the breakthrough of immune checkpoint inhibitor (ICI) in cancer therapy has attracted increasing attention to the immune surveillance within the tumor microenvironment (TME). However, limitations of ICI, such as cancer types, dissatisfactory response, and resistance, suggest that details of the tumor immune surveillance require exploration. Furthermore, it has been proved that some metabolites in TME (such as adenosine, butyrate) could enable cancer cells to fulfill the demand of proliferation and impair the surveillance ability of the immune cells (such as cytotoxicity T cells, natural killer cells), then weakening the efficiency of ICI. Hence, targeting pathways that involve these metabolites have been proposed as a novel strategy to enhance the response of ICI.
It has been found that metabolites derived from cancer cells and those from microbiota display varied effects on tumor immune surveillance. For example, adenosine produced by cancer cells would suppress the activity of immune cells via CD39/CD73/A2AR pathway, while arginine is necessary for the activation of T cells. Moreover, butyrate derived from gut microbiota would directly suppress inflammation to inhibit the development of colon cancer. It is highly significant to uncover more metabolites within TME, both from the cancer cells and the topical microbiota, and their underlying mechanism to regulate the tumor immune surveillance.
This Research Topic will welcome Original Research and Review articles focusing on:
• The interactions between immune cells and cancer metabolites
• The interactions between immune cells and topical microbiota metabolites
• Metabolites within TME that is responsible for tumor progression and immune evasion
• Discovery and development of novel compounds for enhancement of immune checkpoint inhibitors
Important Note: Manuscripts consisting solely of bioinformatics, computational analysis, or predictions of public databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) will not be accepted.
Nowadays, the breakthrough of immune checkpoint inhibitor (ICI) in cancer therapy has attracted increasing attention to the immune surveillance within the tumor microenvironment (TME). However, limitations of ICI, such as cancer types, dissatisfactory response, and resistance, suggest that details of the tumor immune surveillance require exploration. Furthermore, it has been proved that some metabolites in TME (such as adenosine, butyrate) could enable cancer cells to fulfill the demand of proliferation and impair the surveillance ability of the immune cells (such as cytotoxicity T cells, natural killer cells), then weakening the efficiency of ICI. Hence, targeting pathways that involve these metabolites have been proposed as a novel strategy to enhance the response of ICI.
It has been found that metabolites derived from cancer cells and those from microbiota display varied effects on tumor immune surveillance. For example, adenosine produced by cancer cells would suppress the activity of immune cells via CD39/CD73/A2AR pathway, while arginine is necessary for the activation of T cells. Moreover, butyrate derived from gut microbiota would directly suppress inflammation to inhibit the development of colon cancer. It is highly significant to uncover more metabolites within TME, both from the cancer cells and the topical microbiota, and their underlying mechanism to regulate the tumor immune surveillance.
This Research Topic will welcome Original Research and Review articles focusing on:
• The interactions between immune cells and cancer metabolites
• The interactions between immune cells and topical microbiota metabolites
• Metabolites within TME that is responsible for tumor progression and immune evasion
• Discovery and development of novel compounds for enhancement of immune checkpoint inhibitors
Important Note: Manuscripts consisting solely of bioinformatics, computational analysis, or predictions of public databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) will not be accepted.