Existing cancer immunotherapies, such as immune checkpoint inhibitors, therapeutic vaccines, and T cell-based cellular therapies, have significantly improved clinical outcomes in many cancers . However, the response rate to these immunotherapies remains suboptimal, and the mechanisms of resistance are actively being studied.
Bone marrow-derived progenitor cells including mononuclear phagocytes and granulocytes normally develop into several myeloid cell lineages to facilitate innate immune responses but in the context of cancer and other pathological conditions, these cells remain as immature myeloid cells and acquire immunosuppressive activities. These myeloid-derived suppressor cells (MDSCs) impair T-cell -mediated antitumor immune responses thereby impeding the therapeutic outcomes.
This Topical Collection invites studies focused on understanding the molecular mechanisms driving the differentiation and function of MDSCs and developing strategies to reprogram or eliminate MDSCs to enhance antitumor immunity.
We welcome submissions on, but not limited to, the following topics:
1. Tumor-derived factors that promote MDSC metabolism, differentiation, accumulation at tumor sites, and function.
2. MDSC intrinsic molecular signaling pathways that modulate MDSC metabolism, differentiation, migration to tumor sites, and function.
3. Novel suppressive mechanisms of MDSCs, including the control of innate immune cells, Tregs, CD4+ T cells, and CD8+ effector T cells.
4. Novel combinatorial therapies to eliminate or reduce MDSCs, thereby improving the efficacy of current immunotherapies.
Keywords:Myeloid-derived suppressor cells, monocytic MDSCs, polymorphonuclear MDSCs, solid tumor microenvironment, MDSC, myeloid differentiation, resistance mechanisms, combinatorial immunotherapy, Tumor microenvironment, Suppressive myeloid cells, T-cells, T cell suppression