ArticleProceedings of the National Academy of Sciences of the United States of America2011
Severity of innate immune-mediated colitis is controlled by the cytokine deficiency-induced colitis susceptibility-1 (Cdcs1) locus.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 31 citations in OpenAlex.
- Article
- IL-10 Receptor Neutralization-Induced Colitis in Mice: A Comprehensive Guide.Current protocols · 2021Article
- Identification of novel loci controlling inflammatory bowel disease susceptibility utilizing the genetic diversity of wild-derived mice.Genes and immunity · 2020Article
- T-Bet Controls Cellularity of Intestinal Group 3 Innate Lymphoid Cells.Frontiers in immunology · 2020Article
- CARD9 mediates dendritic cell-induced development of Lyn deficiency-associated autoimmune and inflammatory diseases.Science signaling · 2019Article
- Analysis of Cdcs1 colitogenic effects in the hematopoietic compartment reveals distinct microbiome interaction and a new subcongenic interval active in T cells.Mucosal immunology · 2019Article
- Coordination of Immune-Stroma Crosstalk by IL-6 Family Cytokines.Frontiers in immunology · 2019Review
- Alpha kinase 1 controls intestinal inflammation by suppressing the IL-12/Th1 axis.Nature communications · 2018Article
- The JAK inhibitor ruxolitinib reduces inflammation in an ILC3-independent model of innate immune colitis.Mucosal immunology · 2018Article
- An Integrative Framework Reveals Signaling-to-Transcription Events in Toll-like Receptor Signaling.Cell reports · 2017Article
- Characterizing the fecal microbiota of infants with botulism.Microbiome · 2015Article
- A Multihit Model: Colitis Lessons from the Interleukin-10-deficient Mouse.Inflammatory bowel diseases · 2015Review
- CCL2 Promotes Colorectal Carcinogenesis by Enhancing Polymorphonuclear Myeloid-Derived Suppressor Cell Population and Function.Cell reports · 2015Article
- Loss of Gadkin Affects Dendritic Cell Migration In Vitro.PloS one · 2015Article
- Mucosal immune responses following intestinal nematode infection.Parasite immunology · 2014Review
- Nod/Ripk2 signaling in dendritic cells activates IL-17A-secreting innate lymphoid cells and drives colitis in T-bet-/-.Rag2-/- (TRUC) mice.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- The Collaborative Cross as a resource for modeling human disease: CC011/Unc, a new mouse model for spontaneous colitis.Mammalian genome : official journal of the International Mammalian Genome Society · 2014Article
- Genetic analysis of the Trichuris muris-induced model of colitis reveals QTL overlap and a novel gene cluster for establishing colonic inflammation.BMC genomics · 2013Article
- Enhancement of antigen-specific immunoglobulin G responses by anti-CD48.Journal of innate immunity · 2013Article
- Molecular control of steady-state dendritic cell maturation and immune homeostasis.Annual review of immunology · 2013Review
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
Abstract
Genetic modifier loci influence the phenotypic expression of many Mendelian traits; insight into disease pathogenesis gained from their identification in animal disease models may impact the treatment of human multigenic disorders. We previously described an innate immune-driven model of spontaneous ulcerative colitis in T-bet(-/-).Rag2(-/-) double-deficient mice that resembles human ulcerative colitis. On a BALB/c background, this disease is highly penetrant and results in the development of colorectal cancer. However, we observed that colitis in T-bet(-/-).Rag2(-/-) mice on a C57BL/6 background was significantly less severe. Quantitative trait locus analysis using an N2 backcross strategy revealed a single major quantitative trait locus on chromosome 3 that mapped to the Cdcs1 (cytokine deficiency-induced colitis susceptibility-1) locus previously identified in the Il10(-/-) and Gnai2(-/-) colitis models. Congenic introduction of the susceptible Cdcs1 interval from C3H/He into the C57BL/6 background restored colitis severity. Bone marrow reconstitution experiments further mapped the effect of host genetics on disease severity to the hematopoietic compartment. There were distinct differences in the expression of several Cdcs1 genes in bone marrow-derived dendritic cells from Cdcs1 congenic mice. We conclude that the Cdcs1 locus controls colitis severity in T-bet(-/-).Rag2(-/-) mice through innate immune cells.
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