C57BL/6J-Ticam1^Lps2/J

Stock number: 005037
Product name: Trif^Lps2
Research areas: Immunology, Inflammation and Autoimmunity Research, Research Tools

Description

Macrophages in these mice fail to produce tumor necrosis factor (TNF) upon challenge from synthetic lipid A, endotoxin lipopolysaccharide (LPS), and dsRNA. These mice may be useful in studies of immunodeficiency and host response to bacterial endotoxins and viruses.

Detailed description

Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This single base pair deletion mutation was induced by ENU mutagenesis. Unlike wildtype macrophages, macrophages derived from these animals fail to respond to synthetic lipid A, endotoxin lipopolysaccharide (LPS), and dsRNA with production of tumor necrosis factor (TNF). Macrophages are less susceptible to LPS-induced cytotoxicity. Nitrous oxide and type I interferon production in activated macrophages is impaired. Homozygotes exhibit increased susceptibility to mouse cytomegalovirus. Although homozygotes are resistant to challenges with LPS, the mice will become ill and some may die.

Development

This strain was developed using ENU mutagenesis of male C57BL/6 mice. The founding male (#9324) was selected from the F3 generation using a screening protocol for macrophage response to lipid A and endotoxin lopopolyscaccharide (LPS). The ENU treatment induced a single base pair deletion at codon 708.

Allele

Symbol: Ticam1^Lps2
Name: lipopolysaccharide 2
MGI accession ID: MGI:2679794
Generation method: Chemically induced (ENU)
Attributes: Not Specified
Synonyms: Lps; Lps2; Lps2-; Ticam1^-; Ticam1^M1Btlr; TRIF-; Trif^Lps2; Trif^m
Marker symbol: Ticam1
Marker name: toll-like receptor adaptor molecule 1
Marker synonyms: IIAE6; MyD88-3; PRVTIRB; TICAM-1; Trif
Chromosome: 17
Strain of origin: C57BL/6J
Molecular note: ENU mutagenesis induced the deletion of a single guanine within codon 708, resulting in a frameshift mutation. The mutation was predicted to replace 24 C-terminal residues with 11 unrelated residues. The mutation was initially detected by screening macrophages for their competence to respond to LPS.