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. 2018 May 14;9:1039. doi: 10.3389/fimmu.2018.01039

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Copyright © 2018 Prossomariti, Sokol and Ricciardiello.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Effects of nucleotide-binding domain leucine-rich repeat containing (NLR) proteins deficiency on colitis-associated cancer (CAC) development in pre-clinical models. Genetic alterations in NLR proteins result in an increased tumor burden in azoxymethane (AOM)-dextran sulfate sodium (DSS) mouse model of CAC by acting on multiple mechanisms. (A) Deficiency for Asc, Nlrp3, Nlrp6, Casp1, or Il-18 genes led to a dysbiotic microbiota, reduced colonic Il-18 levels, and an impairment of intestinal tissue repair upon injury; (B) Nlrp12; and (C) Nod2 deficiency have been associated with an overgrowth of inflammatory bacteria, enhanced cytokine production, and activation of pro-tumorigenic pathways including NF-kB, MAPK, and Stat3. (D) Knockout for Nlrc3 led to increased colonic inflammation and mTOR signaling activation.