Friend and Foe Alike

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Science  25 Sep 2009:
Vol. 325, Issue 5948, pp. 1601
DOI: 10.1126/science.325_1601b

The immune system protects against infection and disease, but there are numerous examples where it has switched sides, as in autoimmune diseases and in cancer. Cells become cancerous when they acquire genetic mutations that enable them to evade the regular controls on growth. In addition, stomach (Helicobacter pylori) and liver (hepatitis viruses B and C) cancers have been associated with infection-induced inflammation, which involves immune cells, such as macrophages, and inflammation signaling molecules that can promote tumorigenesis. Research on the mechanisms of inflammation-induced carcinogenesis has focused mainly on the innate branch of the immune system, primarily the NF-κB intracellular signaling pathway.

Colorectal cancer has been linked to inflammation of the colon (colitis), which can be caused by bacterial infections. Wu et al. have found that the human bacterium enterotoxigenic Bacteroides fragilis (ETBF), which induces colitis, can promote colon cancer in a mouse model of the disease. They observed that ETBF activated the transcription factor Stat3 and promoted the generation of interleukin-17 (IL-17)–producing T helper cells (TH-17 cells). Blocking IL-17 with neutralizing antibodies inhibited ETBF-induced colon cancer in these mice. Thus, colorectal cancer in humans may be caused by bacterial infection and mediated by a T cell immune response.

Nat. Med. 15, 1016 (2009).

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