ArticleGut2009
Linkage of Crohn's disease-related serological phenotypes: NFKB1 haplotypes are associated with anti-CBir1 and ASCA, and show reduced NF-kappaB activation.
Article in Gut, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Risk association between the NF-κB1 -94ins/delATTG promoter polymorphism and inflammatory bowel diseases: a meta-analysis.Digestive diseases and sciences · 2012Pooled it
- The Current State of Care for Black and Hispanic Inflammatory Bowel Disease Patients.Inflammatory bowel diseases · 2023Review
- Familial Association of Granulocyte-Macrophage Colony-Stimulating Factor Autoantibodies in Inflammatory Bowel Disease.Journal of pediatric gastroenterology and nutrition · 2018Article
- Intraluminal Flagellin Differentially Contributes to Gut Dysbiosis and Systemic Inflammation following Burn Injury.PloS one · 2016Article
- Chronic intestinal inflammation alters hippocampal neurogenesis.Journal of neuroinflammation · 2015Article
- Microbiota activation and regulation of innate and adaptive immunity.Immunological reviews · 2014Review
- Genetics and autoantibodies.Immunologic research · 2013Review
- The CARD8 p.C10X mutation associates with a low anti-glycans antibody response in patients with Crohn's disease.BMC medical genetics · 2013Article
- Beneficial effects of THSG on acetic acid-induced experimental colitis: involvement of upregulation of PPAR-γ and inhibition of the Nf-Κb inflammatory pathway.Molecules (Basel, Switzerland) · 2011Article
- Quantitative trait loci in a bacterially induced model of inflammatory bowel disease.Mammalian genome : official journal of the International Mammalian Genome Society · 2011Article
- Polymorphisms in NF-κB, PXR, LXR, PPARγ and risk of inflammatory bowel disease.World journal of gastroenterology · 2011Article
- Current and future role of biomarkers in Crohn's disease risk assessment and treatment.Clinical and experimental gastroenterology · 2011Article
- High levels of Crohn's disease-associated anti-microbial antibodies are present and independent of colitis in chronic granulomatous disease.Clinical immunology (Orlando, Fla.) · 2011Article
- Cdcs1 a major colitis susceptibility locus in mice; subcongenic analysis reveals genetic complexity.Inflammatory bowel diseases · 2010Article
- Susceptibility to Crohn's disease is mediated by KIR2DL2/KIR2DL3 heterozygosity and the HLA-C ligand.Immunogenetics · 2009Article
- Age of diagnosis influences serologic responses in children with Crohn's disease: a possible clue to etiology?Inflammatory bowel diseases · 2009Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
BACKGROUND AND
aimsGenetics studies of the serum expression of antibodies to microbial antigens may yield important clues to the pathogenesis of Crohn's disease. Our aim was to conduct a linkage study using expression of anti-CBir1, anti-I2, anti-OmpC and ASCA as quantitative traits.
methodsExpression of antibodies to microbial antigens was measured by enzyme-linked immunosorbant assay (ELISA) and a standard approximately 10 cM whole genome microsatellite study was conducted. Single nucleotide polymorphism genotyping was performed using either Illumina or TaqMan MGB technology. Nuclear factor Kappa B (NF-kappaB) activation in cells from Epstein-Barr virus (EBV)-transformed cell lines was assessed using an electrophoretic mobility shift assay and protein was measured using ELISA and western blotting.
resultsEvidence for linkage to anti-CBir1 expression was detected on human chromosome 4 (logarithm of odds (LOD) 1.82 at 91 cM). We therefore directly proceeded to test the association of haplotypes in NFKB1, a candidate gene. One haplotype, H1, was associated with anti-CBir1 (p = 0.003) and another, H3, was associated with ASCA (p = 0.023). Using cell lines from Crohn's disease patients with either H1 or H3, NF-kappaB activation and NF-kappaB p105 and p50 production were significantly lower for patients with H1 compared to patients with H3.
conclusionsThese results suggest that NFKB1 haplotypes induce dysregulation of innate immune responses by altering NF-kappaB expression. The results also show the use of EBV-transformed lymphoblastoid cell lines to conduct phenotypic studies of genetic variation.
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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.