Cancer immunotherapy, especially checkpoint inhibitors, has revolutionized cancer treatment over the last two decades. However, it fails in many patients. While there are many potential reasons for treatment failure, if a T cell response is not present, there is no checkpoint to inhibit. Therefore, it is critical to understand the composition and function of the cells responsible for generating a cancer-associated T cell response. To mount a T cell response, antigen presenting cells (APCs) must acquire, degrade, and present antigen via major histocompatibility complexes to naïve T cells. This process can be inflammatory or inhibitory depending on the signals received by the APC during antigen acquisition. It is now appreciated that in many cancers, especially solid tumors, the tumor microenvironment (TME) can inhibit the APCs ability to acquire and present antigens or to shift the APC towards a more inhibitory phenotype. This results in immunosuppression, rather than immune activation.
The objective of this Research Topic is to evaluate the cellular composition of APCs during cancer immune responses and to interrogate the responses that are generated from these APCs. The current issue is focused on highlighting research on subversion and modulation of the APC by the TME in multiple cancers, research describing the composition of APCs involved, and strategies to increase the APCs ability to mount a productive adaptive immune response.
The current issue is focused on highlighting research on subversion and modulation of the APC by the TME in multiple cancers, research describing the composition of APCs involved, and strategies to increase the APCs' ability to mount a productive adaptive immune response.
We welcome researchers to submit reviews, opinions, or original research focusing on aspects of antigen presentation events during the immune response to cancers.
Manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (clinical cohort or biological validation in vitro or in vivo) are out of scope for this section.
Cancer immunotherapy, especially checkpoint inhibitors, has revolutionized cancer treatment over the last two decades. However, it fails in many patients. While there are many potential reasons for treatment failure, if a T cell response is not present, there is no checkpoint to inhibit. Therefore, it is critical to understand the composition and function of the cells responsible for generating a cancer-associated T cell response. To mount a T cell response, antigen presenting cells (APCs) must acquire, degrade, and present antigen via major histocompatibility complexes to naïve T cells. This process can be inflammatory or inhibitory depending on the signals received by the APC during antigen acquisition. It is now appreciated that in many cancers, especially solid tumors, the tumor microenvironment (TME) can inhibit the APCs ability to acquire and present antigens or to shift the APC towards a more inhibitory phenotype. This results in immunosuppression, rather than immune activation.
The objective of this Research Topic is to evaluate the cellular composition of APCs during cancer immune responses and to interrogate the responses that are generated from these APCs. The current issue is focused on highlighting research on subversion and modulation of the APC by the TME in multiple cancers, research describing the composition of APCs involved, and strategies to increase the APCs ability to mount a productive adaptive immune response.
The current issue is focused on highlighting research on subversion and modulation of the APC by the TME in multiple cancers, research describing the composition of APCs involved, and strategies to increase the APCs' ability to mount a productive adaptive immune response.
We welcome researchers to submit reviews, opinions, or original research focusing on aspects of antigen presentation events during the immune response to cancers.
Manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (clinical cohort or biological validation in vitro or in vivo) are out of scope for this section.
