Recent advances in immunotherapies have led to breakthrough approaches for cancer treatment. Several forms of immunotherapies, including immune checkpoint inhibitors (ICI), T cell transfer therapy, chimeric antigen T cell (CAR-T) therapy, and therapeutic tumor-antigen vaccines, aim to induce an effective and long-lasting T cell-mediated immunity that control cancer progression. However, these approaches have all encountered limitations due to T cell dysfunction.
Among mechanisms that impair tumor-reactive T cells, poor persistence and terminal exhaustion are two inter-connected phenomena that result in short-lived anti-tumor immunity. Recent studies have established that TCF-1-dependent transcriptional program endows memory-like stem-like features to T cells. During acute infection, TCF-1 expression is required for the formation of memory T cells, while parallel in cancer, TCF-1-expressing progenitor-like T cells can self-renewal and differentiate into “exhausted” effector T cells that express inhibitory receptors (i.e., immune checkpoints) and only transiently control tumor growth. It has been demonstrated that successful immunotherapies, including blocking PD-1, rely on inducing a proliferative burst of these stem-like progenitor T cells.
In this thematic issue, we solicit original research articles dissecting the causal mechanisms that regulate the biology of stem-like progenitor T cells. The scope includes but is not limited to studies of next-generation inhibitory receptors, metabolic and cell cycle regulators, or transcriptional networks that influence the formation, expansion, survival, and differentiation of stem-like progenitor-like T cells in the context of anti-tumor immunity.
Manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by robust and relevant validation (clinical cohort or biological validation in vitro or in vivo) are out of scope for this topic.
Keywords:
stem-like T cells, progenitor T cells, memory-like T cells, TCF-1, expansion, differentiation, metabolic quiescence
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
Recent advances in immunotherapies have led to breakthrough approaches for cancer treatment. Several forms of immunotherapies, including immune checkpoint inhibitors (ICI), T cell transfer therapy, chimeric antigen T cell (CAR-T) therapy, and therapeutic tumor-antigen vaccines, aim to induce an effective and long-lasting T cell-mediated immunity that control cancer progression. However, these approaches have all encountered limitations due to T cell dysfunction.
Among mechanisms that impair tumor-reactive T cells, poor persistence and terminal exhaustion are two inter-connected phenomena that result in short-lived anti-tumor immunity. Recent studies have established that TCF-1-dependent transcriptional program endows memory-like stem-like features to T cells. During acute infection, TCF-1 expression is required for the formation of memory T cells, while parallel in cancer, TCF-1-expressing progenitor-like T cells can self-renewal and differentiate into “exhausted” effector T cells that express inhibitory receptors (i.e., immune checkpoints) and only transiently control tumor growth. It has been demonstrated that successful immunotherapies, including blocking PD-1, rely on inducing a proliferative burst of these stem-like progenitor T cells.
In this thematic issue, we solicit original research articles dissecting the causal mechanisms that regulate the biology of stem-like progenitor T cells. The scope includes but is not limited to studies of next-generation inhibitory receptors, metabolic and cell cycle regulators, or transcriptional networks that influence the formation, expansion, survival, and differentiation of stem-like progenitor-like T cells in the context of anti-tumor immunity.
Manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by robust and relevant validation (clinical cohort or biological validation in vitro or in vivo) are out of scope for this topic.
Keywords:
stem-like T cells, progenitor T cells, memory-like T cells, TCF-1, expansion, differentiation, metabolic quiescence
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.