ReviewFrontiers in immunology2026
From gut microbiota-driven mucosal barrier disruption to myeloid-dominant immunosuppressive niches in colorectal cancer.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
Colorectal cancer (CRC) develops within a mucosal ecosystem in which epithelial barrier function, colonizing microbes, inflammatory signaling, and immune cell composition are closely interdependent. Immune checkpoint inhibitors have significantly altered treatment outcomes in patients with mismatch repair-deficient or microsatellite instability-high (dMMR/MSI-H) CRC, but most microsatellite-stable (MSS) tumors still respond poorly, and this is not solely due to lower antigenicity. This article explains this gap mechanistically: gut microbiota dysbiosis weakens the mucosal barrier, promotes microbial translocation, amplifies cytokine and eicosanoid signaling, and remodels the tumor microenvironment into an immunosuppressive state dominated by myeloid cells. We focus on
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