ArticleMammalian genome : official journal of the International Mammalian Genome Society2014
The Collaborative Cross as a resource for modeling human disease: CC011/Unc, a new mouse model for spontaneous colitis.
Article in Mammalian genome : official journal of the International Mammalian Genome Society, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 89 citations in OpenAlex.
- Systems genetics analysis reveals immune mediators of coronavirus disease severity in mice.Genetics · 2026Article
- A New Mouse Model for Ozone Health Effects Research.Environmental health perspectives · 2026Article
- MAIT cells exacerbate colonic inflammation in a genetically diverse murine model of spontaneous colitis.Mucosal immunology · 2025Article
- Crystalline silica exposure induces multiple systemic autoimmune phenotypes including inflammatory arthritis and nephritis in Collaborative Cross mice with differing sub-clinical autoimmune profiles.bioRxiv : the preprint server for biology · 2025Article
- Analysis of Hepatic Lentiviral Vector Transduction: Implications for Preclinical Studies and Clinical Gene Therapy Protocols.Viruses · 2025Article
- Analysis of hepatic lentiviral vector transduction; implications for preclinical studies and clinical gene therapy protocols.bioRxiv : the preprint server for biology · 2024Article
- Collaborative cross strain CC011/UncJ as a novel mouse model of T2-high, severe asthma.Respiratory research · 2023Article
- Which mouse multiparental population is right for your study? The Collaborative Cross inbred strains, their F1 hybrids, or the Diversity Outbred population.G3 (Bethesda, Md.) · 2023Article
- Article
- Using the Collaborative Cross and Diversity Outbred Mice in Immunology.Current protocols · 2022Article
- Genetic Background Matters: Population-Based Studies in Model Organisms for Translational Research.International journal of molecular sciences · 2022Review
- A diversity outbred F1 mouse model identifies host-intrinsic genetic regulators of response to immune checkpoint inhibitors.Oncoimmunology · 2022Article
- The collaborative cross strains and their founders vary widely in cocaine-induced behavioral sensitization.Frontiers in behavioral neuroscience · 2022Article
- A Murine Model of Ozone-induced Nonatopic Asthma from the Collaborative Cross.American journal of respiratory cell and molecular biology · 2021Article
- Patterns and mechanisms of sex ratio distortion in the Collaborative Cross mouse mapping population.Genetics · 2021Article
- Evaluation of Pain and Distress and Therapeutic Interventions for Rectal Prolapse in Mice to Reduce Early Study Removal.Journal of the American Association for Laboratory Animal Science : JAALAS · 2021Article
- Regulation of protein abundance in genetically diverse mouse populations.Cell genomics · 2021Article
- Review
- Quantitative Characterization of Population-Wide Tissue- and Metabolite-Specific Variability in Perchloroethylene Toxicokinetics in Male Mice.Toxicological sciences : an official journal of the Society of Toxicology · 2021Article
- The role of Sp140 revealed in IgE and mast cell responses in Collaborative Cross mice.JCI insight · 2021Article
2 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Inflammatory bowel disease (IBD) is an immune-mediated condition driven by improper responses to intestinal microflora in the context of environmental and genetic background. GWAS in humans have identified many loci associated with IBD, but animal models are valuable for dissecting the underlying molecular mechanisms, characterizing environmental and genetic contributions and developing treatments. Mouse models rely on interventions such as chemical treatment or introduction of an infectious agent to induce disease. Here, we describe a new model for IBD in which the disease develops spontaneously in 20-week-old mice in the absence of known murine pathogens. The model is part of the Collaborative Cross and came to our attention due to a high incidence of rectal prolapse in an incompletely inbred line. Necropsies revealed a profound proliferative colitis with variable degrees of ulceration and vasculitis, splenomegaly and enlarged mesenteric lymph nodes with no discernible anomalies of other organ systems. Phenotypic characterization of the CC011/Unc mice with homozygosity ranging from 94.1 to 99.8% suggested that the trait was fixed and acted recessively in crosses to the colitis-resistant C57BL/6J inbred strain. Using a QTL approach, we identified four loci, Ccc1, Ccc2, Ccc3 and Ccc4 on chromosomes 12, 14, 1 and 8 that collectively explain 27.7% of the phenotypic variation. Surprisingly, we also found that minute levels of residual heterozygosity in CC011/Unc have significant impact on the phenotype. This work demonstrates the utility of the CC as a source of models of human disease that arises through new combinations of alleles at susceptibility loci.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.