Many different populations of immune cells critically contribute to the complex interconnected immunosuppressive networks deployed by tumors to escape from immune detection and elimination. These tumor-induced, tumor-promoting immune populations include cells of the lymphoid lineage (a large variety of immunosuppressive CD4+ and CD8+ “regulatory T lymphocytes”, Tregs), and of myeloid origin (primarily tumor-associated macrophages (TAMs), tumor-associated neutrophils (TANs), tolerogenic dendritic cells (tDC) and immature subsets of myeloid cells endowed with immunosuppressive properties that have collectively been termed “myeloid-derived suppressor cells” (MDSCs)). Induced by different tumor-derived factors, these cells accumulate in the tumor micro-environment, but also at the sites of priming of anti-tumoral immune responses, in the bloodstream and in the metastatic niches. Increased frequency of these cells correlates with a negative prognostic and relapse in many cancer patients.
Characterized by their ability to suppress most anti-tumoral immune effector cells, most of these subsets also exhibit multiple “non-immunological” tumor-promoting functions. Some populations can indeed directly enhance tumor cell survival and proliferation, contribute to the epithelial-to-mesenchymal transition (EMT) and cancer cell stemness, participate in local tissue invasion, foster blood or lymphatic vessel intravasation and extravasation of migrating cancer cells, associate with circulating tumor cells protecting them in the bloodstream and prepare the pre-metastatic niches thus enhancing metastatic processes. Their contribution to cancer cell resistance to chemotherapy and endocrine therapy has also been described, making them potential therapeutic targets.
In the current Research Topic, we welcome the submission of Original Research articles, Reviews, Mini Reviews, Hypotheses and Theory, Perspectives and expert Opinions on subjects addressing the identification, multifaceted roles and therapeutic manipulations of these cells, including, but not limited to:
1. Characterizing the immunosuppressive myeloid landscape at single-cell sequencing level and identifying novel markers to better discriminate and specifically target these cells in cancers.
2. Addressing current challenges related to the ambiguous identification of phenotypically and functionally distinct subsets of myeloid suppressive cells in the tumor environment.
3. Identification and therapeutic targeting of the mechanisms and pathways responsible for the development and functions of tumor-promoting immune cell populations.
4. Assessing the high degree of plasticity of myeloid cells and/or Tregs in relation to the possible therapeutic reprogramming of these cells.
5. Characterizing the importance of the cross-talks between tumor-promoting myeloid cells or Treg and stromal cells, such as cancer-associated fibroblasts, in the tumor environment.
Many different populations of immune cells critically contribute to the complex interconnected immunosuppressive networks deployed by tumors to escape from immune detection and elimination. These tumor-induced, tumor-promoting immune populations include cells of the lymphoid lineage (a large variety of immunosuppressive CD4+ and CD8+ “regulatory T lymphocytes”, Tregs), and of myeloid origin (primarily tumor-associated macrophages (TAMs), tumor-associated neutrophils (TANs), tolerogenic dendritic cells (tDC) and immature subsets of myeloid cells endowed with immunosuppressive properties that have collectively been termed “myeloid-derived suppressor cells” (MDSCs)). Induced by different tumor-derived factors, these cells accumulate in the tumor micro-environment, but also at the sites of priming of anti-tumoral immune responses, in the bloodstream and in the metastatic niches. Increased frequency of these cells correlates with a negative prognostic and relapse in many cancer patients.
Characterized by their ability to suppress most anti-tumoral immune effector cells, most of these subsets also exhibit multiple “non-immunological” tumor-promoting functions. Some populations can indeed directly enhance tumor cell survival and proliferation, contribute to the epithelial-to-mesenchymal transition (EMT) and cancer cell stemness, participate in local tissue invasion, foster blood or lymphatic vessel intravasation and extravasation of migrating cancer cells, associate with circulating tumor cells protecting them in the bloodstream and prepare the pre-metastatic niches thus enhancing metastatic processes. Their contribution to cancer cell resistance to chemotherapy and endocrine therapy has also been described, making them potential therapeutic targets.
In the current Research Topic, we welcome the submission of Original Research articles, Reviews, Mini Reviews, Hypotheses and Theory, Perspectives and expert Opinions on subjects addressing the identification, multifaceted roles and therapeutic manipulations of these cells, including, but not limited to:
1. Characterizing the immunosuppressive myeloid landscape at single-cell sequencing level and identifying novel markers to better discriminate and specifically target these cells in cancers.
2. Addressing current challenges related to the ambiguous identification of phenotypically and functionally distinct subsets of myeloid suppressive cells in the tumor environment.
3. Identification and therapeutic targeting of the mechanisms and pathways responsible for the development and functions of tumor-promoting immune cell populations.
4. Assessing the high degree of plasticity of myeloid cells and/or Tregs in relation to the possible therapeutic reprogramming of these cells.
5. Characterizing the importance of the cross-talks between tumor-promoting myeloid cells or Treg and stromal cells, such as cancer-associated fibroblasts, in the tumor environment.
