Il10 Knockout (BALB/c)

Constitutive Knockout

Il10 Knockout (BALB/c) Mice - Constitutive Knockout - Taconic Biosciences

BALB/cAnNTac Background

  • Model #
  • Genotype
  • Nomenclature
  • 15660-F
    ko/ko
    BALB/cAnNTac-Il10em7Tac
  • 15660-M
    ko/ko
    BALB/cAnNTac-Il10em7Tac
  • Useful for studying colitis and immunoregulatory pathways
  • Carries a deletion of the entire Il10 coding sequence
  • Homozygous mice do not produce the anti-inflammatory cytokine IL-10
  • Colitis severity and onset are expected to vary by genetic background in Il10 knockouts, with reported earlier onset and greater severity in BALB/c vs. C57BL/6 backgrounds (J Clin Invest. 1996 Aug 15;98(4):1010-20)
  • Colitis in this model is highly microbiome-dependent; disease severity and age of onset will be affected by different facility microbiomes (Infect Immun. 1998 Nov;66(11):5224-31)
  • Although germ-free Il10 knockouts do not develop colitis (Infect Immun. 1998 Nov;66(11):5224-31), the introduction of select microbes or fecal microbiomes induces rapid colitis onset in adult animals (Inflamm Bowel Dis. 2007 Dec;13(12):1457-66).
  • Available at the Germ Free and Excluded Flora health standards to enable microbiome research
  • Order model #15660 for Excluded Flora or model #GF-15660 for Germ Free
  • Phenotype update: Feedback from a pharma customer who received female 15660 mice from Taconic is that spontaneous colitis occurred in all vehicle treated animals. The disease progressed slowly without remission, with clinical onset at 15 wk of age until study termination at 20 wk of age. A clinically-relevant drug treatment was effective in reducing disease progression.
Orders by weight: Taconic cannot accept orders by weight for this model. Please note that shipments may contain animals with a larger weight variation.

Availability: EF animals available now. GF animals expected to be available in late 2018/early 2019.

Genetic Background:

BALB/cAnNTac Background

Origin:

The Il10 knockout mouse was developed by Taconic Biosciences. The model was created through CRISPR/Cas9-mediated gene editing to delete the entire Il10 locus (exons 1 to 5, including the proximal promoter and UTRs).  Targeting occurred in BALB/cAnNTac embryos.  The selected G1 founder was screened for off-target effects and the targeted locus was sequenced to confirm targeting specificity.  Heterozygous animals were intercrossed to generate homozygous mice. The line is maintained by incrossing homozygous mice.

Color:

Albino

Species:

Mouse

Initial Publication:

There is no specific publication describing the generation of these mice, but multiple publications exist demonstrating applications using similar models. See reference list.

Other Publications:

Kühn R, Löhler J, Rennick D, Rajewsky K, Müller W. Interleukin-10-deficient mice develop chronic enterocolitis. Cell. 1993 Oct 22;75(2):263-74.

Berg DJ, Davidson N, Kühn R, Müller W, Menon S, Holland G, Thompson-Snipes L, Leach MW, Rennick D. Enterocolitis and colon cancer in interleukin-10-deficient mice are associated with aberrant cytokine production and CD4(+) TH1-like responses. J Clin Invest. 1996 Aug 15;98(4):1010-20.

Sellon RK, Tonkonogy S, Schultz M, Dieleman LA, Grenther W, Balish E, Rennick DM, Sartor RB. Resident enteric bacteria are necessary for development of spontaneous colitis and immune system activation in interleukin-10-deficient mice. Infect Immun. 1998 Nov;66(11):5224-31.

Kim SC, Tonkonogy SL, Karrasch T, Jobin C, Sartor RB. Dual-association of gnotobiotic IL-10-/- mice with 2 nonpathogenic commensal bacteria induces aggressive pancolitis. Inflamm Bowel Dis. 2007 Dec;13(12):1457-66.


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Phenotype update: Feedback from a pharma customer who received female 15660 mice from Taconic is that spontaneous colitis occurred in all vehicle treated animals. The disease progressed slowly without remission, with clinical onset at 15 wk of age until study termination at 20 wk of age. A clinically-relevant drug treatment was effective in reducing disease progression.