Table 3. Susceptibility to colitis-associated tumor in PRR knockout mice.
| PRR knockouts | Susceptibility | Possible pathogenesis |
|---|---|---|
| TLRs | ||
| TLR2105 | Increased | Increased epithelial proliferation due to greater expression of tumorigenic cytokines and epithelial STAT3 activation |
| TLR456, 59, 104 | Decreased | Defective mucosal expression of COX-2 and following production of PGE2. Defective mucosal production of EGFR ligand, amphiregulin |
| NLRs | ||
| NOD172 | Increased | Increased intestinal inflammation and greater expression of tumorigenic cytokines resulting in epithelial proliferation |
| NOD2117 | Increased | Transmissible by co-housing (The pathogeneis involves commensal bacteria) |
| NLRC4114 | Increased/the other report shows similar susceptibility to WT mice | Defective caspase-1 activation resulting in protection of epithelial cells from apoptosis |
| NLRP376 | Increased | Defective caspase-1 activation. Defective mucosal IL-18 release |
| NLRP661, 62 | Increased | Increased expression of Wnt-target genes. Defective mucosal IL-18 release |
| NLRP12115, 116 | Increased | Increased intestinal inflammation and greater expression of tumorigenic cytokines. Increased epithelial proliferation |
COX-2, cyclooxygenase 2; EGFR, epidermal growth factor receptor; IL, interleukin; NLR, nucleotide-binding oligomerization domain (NOD)-like receptor; NLRP, NLR protein; PGE2, prostaglandin E2; PRR, pattern-recognition receptor; STAT3, signal transducer and activator of transcription factor 3; TLR, Toll-like receptor; WT, wild type.