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. Author manuscript; available in PMC: 2016 May 21.
Published in final edited form as: Adv Cancer Res. 2015 May 21;128:235–262. doi: 10.1016/bs.acr.2015.04.011

Figure 2. Commensal microbiota differentially influence the tumor environment and immunotherapy.

Figure 2

A) The influence of TLR5 expression on tumor progression. TLR5 responsive hosts have accelerated tumor progression in the presence of an IL-6 responsive tumor, resulting in increased levels of IL-6, increased recruitment of MDSCs into the tumor environment, and the induction of galectin-1 expression in tumor-associated γδ T cells. TLR5-deficient hosts have elevated levels of IL-17, which in the absence of IL-6, drives tumor progression. B) Commensal microbiota are required for effective immunotherapy with CpG and anti-IL-10R antibody treatment to reverse the immune suppression of tumor-associated DCs. The commensal microbiota prime DCs through TLR4 interaction, resulting in production of TNFα in response to CpG treatment. This results in conversion of suppressed DCs into immunostimulatory DCs, which elicit anti-tumor immunity. C) The effects of cyclophosphamide are mediated through the microbiota. Cyclophosphamide disrupts the mucosal surface, allowing for bacterial translocation to distal lymph organs, such as the spleen. This results in the conversion of IL-17 producing Th cells, which enhance anti-tumor immune response.