ArticleArthritis research & therapy2011
A polymorphism in the interleukin-4 receptor affects the ability of interleukin-4 to regulate Th17 cells: a possible immunoregulatory mechanism for genetic control of the severity of rheumatoid arthritis.
Article in Arthritis research & therapy, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Association of Interleukin-4 Receptor α Chain I50V Gene Variant (rs1805010) and Asthma in Iranian Population: A Case-control Study.The open respiratory medicine journal · 2024Article
- Review
- Relapsing-remitting multiple sclerosis arising in a patient with atopic dermatitis on dupilumab.JAAD case reports · 2021Article
- Anti-Inflammatory Therapeutic Approaches to Prevent or Delay Post-Traumatic Osteoarthritis (PTOA) of the Knee Joint with a Focus on Sustained Delivery Approaches.International journal of molecular sciences · 2021Review
- Review: Transcriptional Regulation of CD4+ T Cell Differentiation in Experimentally Induced Arthritis and Rheumatoid Arthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2018Review
- IL-4Rα Polymorphism Is Associated With Myasthenia Gravis in Chinese Han Population.Frontiers in neurology · 2018Article
- Interaction among activated lymphocytes and mesenchymal cells through podoplanin is critical for a high IL-17 secretion.Arthritis research & therapy · 2016Article
- Commentary: IL-4 and IL-13 receptors and signaling.Cytokine · 2015Article
- Gene network inference using continuous time Bayesian networks: a comparative study and application to Th17 cell differentiation.BMC bioinformatics · 2014Article
- Association of the IL4R single-nucleotide polymorphism I50V with recurrent spontaneous abortion (RSA).Journal of assisted reproduction and genetics · 2014Article
- The effect of IL-4 gene polymorphisms on cytokine production in patients with chronic periodontitis and in healthy controls.Mediators of inflammation · 2014Article
- Article
- Protective effects of interleukin-4 on tissue destruction and morphological changes of bovine nasal chondrocytes in vitro.Iranian biomedical journal · 2013Article
- IL-23R rs11209026 polymorphism modulates IL-17A expression in patients with rheumatoid arthritis.Genes and immunity · 2012Article
- Deciphering the role of Th17 cells in human disease.Trends in immunology · 2011Review
- Interleukin 17 as a novel predictor of vascular function in rheumatoid arthritis.Annals of the rheumatic diseases · 2011Article
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7 authors.
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Abstract
introductionRheumatoid arthritis (RA) is now suspected to be driven by pathogenic Th17 cells that secrete interleukin (IL)-17 and can be regulated by IL-4. A single-nucleotide polymorphism (SNP), I50V, in the coding region of the human IL-4 receptor (IL-4R) is associated with rapid development of erosive disease in RA. The present study was undertaken to determine whether this SNP renders the IL-4R less able to transduce signals that regulate IL-17 production.
methodsPeripheral blood mononuclear cells were activated under Th17-stimulating conditions in the presence or absence of IL-4, and IL-17 production was measured by both enzyme-linked immunosorbent assay (ELISA) and flow cytometry. Serum IL-17 was also measured by ELISA. Paired comparisons were performed using the two-tailed t-test. IL-4 receptor gene alleles were determined by polymerase chain reaction.
resultsIn healthy individuals, IL-4 significantly inhibited IL-17 production by cells from subjects with the I/I genotype (P = 0.0079) and the I/V genotype (P = 0.013), but not the V/V genotype (P > 0.05). In a cross-sectional sample of patients with established RA, the magnitude of the in vitro effect of IL-4 was lower and was not associated with a specific IL-4R allele. Serum IL-17 levels were higher in RA patients than in healthy individuals, as was the percentage of CD4+ cells that produced IL-17.
conclusionsThese results indicate that an inherited polymorphism of the IL-4R controls the ability of the human immune system to regulate the magnitude of IL-17 production. However, in established RA, this pattern may be altered, possibly due to secondary effects of both RA itself as well as immunomodulatory medications. Ineffective control of Th17 immune responses is a potential mechanism to explain why IL-4R is an important severity gene in RA, but this issue will require careful study of a cohort of new-onset RA patients.
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