The Tlr5 gene encodes toll-like receptor 5, which has a fundamental role in bacteria recognition and activation of innate immune responses. TLR5 is the receptor for bacterial flagellin, and then acts via MYD88 and TRAF6; leading to NF-kappa-B activation, cytokine secretion and the inflammatory response.
The Tlr5fl allele has loxP sites flanking exon 4 of the Tlr5 gene. Mice homozygous for the Tlr5fl allele are viable and fertile with no reported abnormalities. When bred to mice that express Cre recombinase, the resulting offspring will have absence of Tlr5 function in cre-expressing tissues. Examples listed below.
When bred to germline Cre-expressing mice (Stock No. 006054), the resulting Tlr5 global knockout homozygotes are expected to exhibit increased levels of flagellated bacteria in the intestine, that will promote low-grade inflammation, metabolic syndrome and colitis.
When Tlr5fl mice are bred to Villin-Cre transgenic mice (Stock No. 004586), the resulting Tlr5ΔIEC homozygotes lack TLR5 expression in intestinal intraepithelial cells, and exhibit a phenotype similar to global TLR5 knockout mice.
When Tlr5fl mice are bred to Cd11c-Cre transgenic mice (Stock No. 007567), the resulting Tlr5ΔDC homozygotes lack TLR5 expression in dendritic cells, and exhibit complete loss of flagellin-induced production of interleukin-22, but do not develop an inflammation-associated phenotype or an altered microbiota composition, as seen in Tlr5ΔIEC and in global TLR5 knockout mice.
