ArticleThe Journal of biological chemistry2016
IL23R (Interleukin 23 Receptor) Variants Protective against Inflammatory Bowel Diseases (IBD) Display Loss of Function due to Impaired Protein Stability and Intracellular Trafficking.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
54 citing papers in PubMed, 1 synthesis or guideline pooled it, 90 citations in OpenAlex.
- Interleukin-23 Receptor and Interleukin-17 Receptor A: Splice Variants, Isoforms and Their Relationship With Periodontitis-A Systematic Review and Bioinformatic Analysis.Journal of cellular and molecular medicine · 2026Pooled it
- Review
- In Silico Identification and Structural Characterization of High-Risk Missense SNVs in the HumanGenes · 2026Article
- Overexpression of the IL-23/IL-17A Axis and Their Receptors (IL-23R and IL-17RA) in Gingival Tissue of Patients With Periodontitis.International journal of dentistry · 2026Article
- Multi-omic insights from a multi-ancestry genome-wide meta-analysis of ankylosing spondylitis reveal novel pathways of disease susceptibility.Research square · 2025Article
- Targeting the IL-23 Receptor Gene: A Promising Approach in Inflammatory Bowel Disease Treatment.International journal of molecular sciences · 2025Review
- Interpreting the Function of the IL-23/IL-17 Axis through Bioinformatics.Endocrine, metabolic & immune disorders drug targets · 2025Review
- The IL-23R and Its Genetic Variants: A Hitherto Unforeseen Bridge Between the Immune System and Cancer Development.Cancers · 2024Review
- [Old and New Biologics and Small Molecules in Inflammatory Bowel Disease: Anti-interleukins].The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi · 2024Review
- The Contribution of Genetic and Epigenetic Factors: An Emerging Concept in the Assessment and Prognosis of Inflammatory Bowel Diseases.International journal of molecular sciences · 2024Review
- Inflammatory Bowel Disease: A Comprehensive Analysis of Molecular Bases, Predictive Biomarkers, Diagnostic Methods, and Therapeutic Options.International journal of molecular sciences · 2024Review
- Diagnosis and Management of Infections in Patients with Mendelian Susceptibility to Mycobacterial Disease.Pathogens (Basel, Switzerland) · 2024Review
- The Genetics of Inflammatory Bowel Disease.Molecular diagnosis & therapy · 2024Review
- IL-12 and IL-23 pathway inhibition in inflammatory bowel disease.Nature reviews. Gastroenterology & hepatology · 2023Review
- The Role of IL-23 in the Pathogenesis and Therapy of Inflammatory Bowel Disease.International journal of molecular sciences · 2023Review
- Use of NanoBiT and NanoBRET to characterise interleukin-23 receptor dimer formation in living cells.British journal of pharmacology · 2023Article
- Article
- Characterisation of IL-23 receptor antagonists and disease relevant mutants using fluorescent probes.Nature communications · 2023Article
- Kernel-based genetic association analysis for microbiome phenotypes identifies host genetic drivers of beta-diversity.Microbiome · 2023Article
- Longitudinal DNA methylation profiling of the rectal mucosa identifies cell-specific signatures of disease status, severity and clinical outcomes in ulcerative colitis cell-specific DNA methylation signatures of UC.Clinical epigenetics · 2023Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Genome-wide association studies as well as murine models have shown that the interleukin 23 receptor (IL23R) pathway plays a pivotal role in chronic inflammatory diseases such as Crohn disease (CD), ulcerative colitis, psoriasis, and type 1 diabetes. Genome-wide association studies and targeted re-sequencing studies have revealed the presence of multiple potentially causal variants of the IL23R. Specifically the G149R, V362I, and R381Q IL23Rα chain variants are linked to protection against the development of Crohn disease and ulcerative colitis in humans. Moreover, the exact mechanism of action of these receptor variants has not been elucidated. We show that all three of these IL23Rα variants cause a reduction in IL23 receptor activation-mediated phosphorylation of the signal-transducing activator of transcription 3 (STAT3) and phosphorylation of signal transducing activator of transcription 4 (STAT4). The reduction in signaling is due to lower levels of cell surface receptor expression. For G149R, the receptor retention in the endoplasmic reticulum is due to an impairment of receptor maturation, whereas the R381Q and V362I variants have reduced protein stability. Finally, we demonstrate that the endogenous expression of IL23Rα protein from V362I and R381Q variants in human lymphoblastoid cell lines exhibited lower expression levels relative to susceptibility alleles. Our results suggest a convergent cause of IL23Rα variant protection against chronic inflammatory disease.
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