Myeloid-derived suppressor cells across the intestinal inflammation-colorectal cancer continuum: From immune regulation to immune escape

Myeloid-derived suppressor cells (MDSCs) comprise heterogeneous myeloid populations whose phenotype and suppressive function depend on disease stage, subset, tissue compartment, and local signals.This narrative review examines their roles across intestinal inflammation, inflammatory bowel disease (IBD), colitis-associated carcinogenesis (CAC), colorectal cancer (CRC), and immune escape.It emphasizes evidence source and directness, particularly in microsatellite-stable (MSS) CRC.Primary intestinal-disease studies, human tissue investigations, and mechanistic animal interventions were prioritized over marker-only descriptions and extraintestinal extrapolation.Experimental colitis studies show that suppressive myeloid populations can restrain tissue injury, whereas persistent inflammation may favor abnormal recruitment and impaired immune surveillance.These effects are context-dependent and are not determined by disease duration alone.Mechanistic evidence for the IBD-CAC transition remains predominantly murine, with limited longitudinal human validation.In established CRC, human studies demonstrate compartment-specific associations and suppressive activity in selected populations.Many recruitment pathways and therapeutic combinations nevertheless remain preclinical.The evidence supports interpreting MDSCs through disease stage, subset identity, tissue compartment, and measured function.MDSC-directed interventions in IBD, CAC, and MSS CRC remain investigational and require validated biomarkers and intervention windows rather than indiscriminate expansion or depletion.