fig2

From gut-liver axis hijacking to intratumoral microbiota establishment: mechanisms and therapeutic opportunities in hepatocellular carcinoma

Figure 2. Intratumoral microbiota and gut microbiotaderived factors exert opposing effects on the TIME. (A) Immunosuppression: Intratumoral bacteria such as K. pneumoniae, S. anginosus, and E. faecalis promote an immunosuppressive microenvironment by modulating immune cell functions, including inhibiting the activity of NKT cells, increasing the infiltration of Th1, Th2, and Th17 cells, recruiting MDSCs, and impairing the proliferation of CD8+ T cells, leading to HCC progression; (B) Immunoactivation: Intestinal microbiota that can influence the TIME, such as A. muciniphila, activate anti-tumor immunity by stimulating CD8+ T cells and reducing Treg infiltration, leading to HCC regression. HCC: Hepatocellular carcinoma; TIME: tumor immune microenvironment; NKT: natural killer T cell; Th: T helper cell; MDSC: myeloid-derived suppressor cell; Treg: regulatory T cell.

Hepatoma Research
ISSN 2454-2520 (Online) 2394-5079 (Print)

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