The role of myeloid-derived suppressor cells in lung cancer

Abstract

Background: Lung cancer remains one of the leading causes of cancer-related mortality worldwide. Immune evasion and chronic inflammation are central determinants of tumor progression and therapeutic resistance. We aimed to analyze recent scientific literature addressing the role of myeloid-derived suppressor cells (MDSCs) in lung cancer, focusing on their mechanisms of action and clinical relevance. Methods: An integrative literature review was conducted using the PubMed and Virtual Health Library (BVS) databases, employing the descriptors “Myeloid-Derived Suppressor Cells” and “Lung Neoplasms.” The search was restricted to English-language articles published between 2020 and 2025. Study selection followed the PRISMA guidelines, resulting in a final sample of 61 original studies. Results: Evidence indicates that MDSCs—particularly the polymorphonuclear (PMN-MDSC) and monocytic (M-MDSC) subsets—are actively recruited to the tumor microenvironment by chemokines such as CCL2 and CXCL5. These cells exert potent immunosuppressive effects through the production of reactive oxygen species (ROS), arginase-1, and the expression of PD-L1, leading to inhibition of cytotoxic T lymphocytes and natural killer cells. Elevated MDSC levels were consistently associated with poor prognosis, metastatic progression, and resistance to therapies, including immune checkpoint inhibitors and targeted treatments. Conclusion: MDSCs function as central regulators of tumor aggressiveness and constitute major barriers to effective anticancer immunity. Current literature supports the targeting of MDSC depletion or functional reprogramming as a promising strategy to overcome immunosuppression and improve clinical outcomes in lung cancer.