ArticlePloS one2009
Genetic association analysis of the functional c.714T>G polymorphism and mucosal expression of dectin-1 in inflammatory bowel disease.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 44 citations in OpenAlex.
- The CLEC7A Y238∗ variant and susceptibility to pneumonia: a prospective population-based cohort study and mechanistic investigation.EBioMedicine · 2026Article
- C-Type lectin receptors as key modulators of intestinal inflammation: insights into IBD pathogenesis and therapy.FEMS microbiology letters · 2026Review
- Dectin-1 as a therapeutic target for inflammatory bowel disease.Advances in pharmacology (San Diego, Calif.) · 2024Review
- Article
- Circulating 1,3-Beta-D-Glucan is Associated with Lung Function, Respiratory Symptoms, and Mediators of Matrix Degradation in Chronic Obstructive Pulmonary Disease.Chronic obstructive pulmonary diseases (Miami, Fla.) · 2022Article
- Antifungal immunity mediated by C-type lectin receptors may be a novel target in immunotherapy for urothelial bladder cancer.Frontiers in immunology · 2022Article
- The Role of C-Type Lectin Receptor Signaling in the Intestinal Microbiota-Inflammation-Cancer Axis.Frontiers in immunology · 2022Review
- The role of mycobiota-genotype association in inflammatory bowel diseases: a narrative review.Gut pathogens · 2021Review
- Effects of Dietary Oat Beta-Glucans on Colon Apoptosis and Autophagy through TLRs and Dectin-1 Signaling Pathways-Crohn's Disease Model Study.Nutrients · 2021Article
- Inflammatory Bowel Diseases: Host-Microbial-Environmental Interactions in Dysbiosis.Diseases (Basel, Switzerland) · 2020Review
- Topical Therapy with Antisense Tumor Necrosis Factor Alpha Using Novel β-Glucan-Based Drug Delivery System Ameliorates Intestinal Inflammation.International journal of molecular sciences · 2020Article
- Myeloid C-type lectin receptors in skin/mucoepithelial diseases and tumors.Journal of leukocyte biology · 2019Review
- Studying fungal pathogens of humans and fungal infections: fungal diversity and diversity of approaches.Genes and immunity · 2019Review
- Fungal dysbiosis: immunity and interactions at mucosal barriers.Nature reviews. Immunology · 2017Review
- The Correlation of CD206, CD209, and Disease Severity in Behçet's Disease with Arthritis.Mediators of inflammation · 2017Article
- Surgical diverticulitis is not associated with defects in the expression of wound healing genes.International journal of colorectal disease · 2015Article
- Mycobiota in gastrointestinal diseases.Nature reviews. Gastroenterology & hepatology · 2015Review
- Autophagy: a new target or an old strategy for the treatment of Crohn's disease?Nature reviews. Gastroenterology & hepatology · 2013Review
- Candida albicans primes TLR cytokine responses through a Dectin-1/Raf-1-mediated pathway.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- A new therapeutic approach using a schizophyllan-based drug delivery system for inflammatory bowel disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2012Article
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDectin-1 is a pattern recognition receptor (PRR) expressed by myeloid cells that specifically recognizes beta-1,3 glucan, a polysaccharide and major component of the fungal cell wall. Upon activation, dectin-1 signaling converges, similar to NOD2, on the adaptor molecule CARD9 which is associated with inflammatory bowel disease (IBD). An early stop codon polymorphism (c.714T>G) in DECTIN-1 results in a loss-of-function (p.Y238X) and impaired cytokine responses, including TNF-alpha, interleukin (IL)-1beta and IL-17 upon in vitro stimulation with Candida albicans or beta-glucan. The aim of the present study was to test the hypothesis that the DECTIN-1 c.714T>G (p.Y238X) polymorphism is associated with lower disease susceptibility or severity in IBD and to investigate the level of dectin-1 expression in inflamed and non-inflamed colon tissue of IBD patients. METHODOLOGY: Paraffin embedded tissue samples from non-inflamed and inflamed colon of IBD patients and from diverticulitis patients were immunohistochemically stained for dectin-1 and related to CD68 macrophage staining. Genomic DNA of IBD patients (778 patients with Crohn's disease and 759 patients with ulcerative colitis) and healthy controls (n = 772) was genotyped for the c.714T>G polymorphism and genotype-phenotype interactions were investigated. PRINCIPAL
findingsIncreased expression of dectin-1 was observed in actively inflamed colon tissue, as compared to non-inflamed tissue of the same patients. Also an increase in dectin-1 expression was apparent in diverticulitis tissue. No statistically significant difference in DECTIN-1 c.714T>G allele frequencies was observed between IBD patients and healthy controls. Furthermore, no differences in clinical characteristics could be observed related to DECTIN-1 genotype, neither alone, nor stratified for NOD2 genotype.
conclusionsOur data demonstrate that dectin-1 expression is elevated on macrophages, neutrophils, and other immune cells involved in the inflammatory reaction in IBD. The DECTIN-1 c.714T>G polymorphism however, is not a major susceptibility factor for developing IBD.
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