Table 2. Intestinal phenotypes and their susceptibility to colitis in PRR knockout mice.
| PRR target | Gene modification | Intestinal phenotypes |
|---|---|---|
| TLRs | ||
| TLR249, 52 | Knockout | Increased susceptibility to DSS colitis |
| TLR439, 49, 50 | Knockout | Increased susceptibility to DSS colitis. Exacerbate or ameliorate IL-10−/− colitis (depending on commensals or Helicobacter hepaticus) |
| TLR5a,25, 43 | Knockout | Spontaneous colitis (25%), increased susceptibility to DSS colitis |
| TLR960, 140 | Knockout | Increased susceptibility to DSS acute colitis but resistant to chronic DSS colitis |
| NLRs | ||
| NOD172, 73 | Knockout | Increased susceptibility to DSS colitis |
| NOD215, 68, 69, 71 | Knockout | Increased susceptibility to DSS colitis and TNBS colitis. Defective cryptdin expression |
| Knock-in of human NOD2-3020insC mutation | Increased susceptibility to bacterial-induced intestinal inflammation | |
| NLRC4114 | Knockout | Similar susceptibility to DSS colitis as WT mice |
| NLRP374, 75, 76, 77, 81, 82 | Knockout | Increased or reduced susceptibility to DSS colitis (depending on the reports). Increased or reduced susceptibility to TNBS colitis |
| NLRP6a,27, 61, 62 | Knockout | Spontaneous colitis (crypt hyperplasia and inflammatory cell recruitment), increased susceptibility to DSS colitis |
| RNA helicases | ||
| RIG-Ia,26 | Knockout | Spontaneous intestinal inflammation |
DSS, dextran sulfate sodium; IL, interleukin; NLR, nucleotide-binding oligomerization domain (NOD)-like receptor; NLRP, NLR protein; PRR, pattern-recognition receptor; RIG-I, retinoid acid-inducible gene-I; TLR, Toll-like receptor; TNBS, 2,4,6-trinitrobenzenesulfonic acid; WT, wild type.
aSpontaneous phenotype.