- 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 may induce rapid colitis onset in adult animals (Inflamm Bowel Dis. 2007 Dec;13(12):1457-66).
- Available at the Germ Free health standard to enable microbiome research. Order model #GF-16006.
Guidance for selecting the most appropriate Il10 Knockout model for your research:- The BALB/c Il10 Knockout at the Opportunist Free health standard (Taconic model #15660) is appropriate for studies involving rapid spontaneous disease onset. This model may be best for routine screening of new colitis therapeutics.
- The C57BL/6 Il10 Knockout is no longer available at the Opportunist Free health standard, but Germ Free mice can be associated with your flora of choice. It can also be used for crossbreeding to other GEMs on the C57BL/6 background, for example to study whether crossing to a particular knockout results in more or less severe disease as an insight into IBD mechanisms. Inquire for details on a crossbreeding license.
- The Germ Free Il10 Knockout is the most appropriate model for microbiome studies, including investigations of mono-associations, specific complex microbiota compositions or patient-derived microbiota samples. Association of Germ Free Il10 Knockout mice can provide cohorts which develop accelerated and synchronized disease, which may cut down the timeline for drug screening.
Orders by weight: Taconic cannot accept orders by weight for this model. Please note that shipments may contain animals with a larger weight variation.
Genetic Background:
C57BL/6NTac 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 C57BL/6NTac 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.
Genetics:
Wild type for Nnt mutation
Color:
Black 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.
