Fusobacterium nucleatum is an identified proinflammatory autochthonous bacterium implicated in human colorectal cancer. It is also abundantly found in patients suffering from chronic gut inflammation (inflammatory bowel disease), consequently contributing to the pathogenesis of colorectal cancer. Majority of the studies have reported that colorectal tumors/colorectal adenocarcinomas are highly enriched with F. nucleatum compared to noninvolved adjacent colonic tissue. During the course of multistep development of colorectal cancer, tumors have evolved many mechanisms to resist the antitumor immune response. One of such favorite ploy is providing access to pathogenic bacteria, especially F. nucleatum in the colorectal tumor microenvironment, wherein both (colorectal tumors and F. nucleatum) exert profound effect on each other, consequently attracting tumor-permissive myeloid-derived suppressor cells, suppressing cytotoxic CD8+ T cells and inhibiting NK cell-mediated cancer cell killing. In this review, we have primarily focused on how this bug modulates the immune response, consequently rendering the antitumor immune cells inactive.
Fusobacterium nucleatum (F. nucleatum) Inflammatory bowel disease (IBD) Crohn’s disease (CD) Ulcerative colitis (UC) T cell immunoglobulin and ITIM (TIGIT) domain
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The authors gratefully acknowledge the support provided by University of Kashmir, Srinagar. The contributions made by Mudassir Habib, Samirul Bashir, and Nazia Hilal from the Department of Biotechnology, University of Kashmir are acknowledged.
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Conflicts of interest
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