ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Posttranscriptional gene regulation of IL-17 by the RNA-binding protein HuR is required for initiation of experimental autoimmune encephalomyelitis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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Who cites it
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.
- Long Non-Coding RNAs, Novel Offenders or Guardians in Multiple Sclerosis: A Scoping Review.Frontiers in immunology · 2021Pooled it
- Targeting RNA binding proteins with small-molecule inhibitors: Advances, challenges, and therapeutic opportunities.Acta pharmaceutica Sinica. B · 2026Review
- Heat-killedResearch square · 2026Article
- Multifaceted Nature of HuR in Atherosclerosis Development.Current medicinal chemistry · 2025Review
- PEGylated Peptide for Targeted Inhibition of Human Antigen R as a Novel Therapeutic Strategy for Psoriasis: A Proof-of-Concept Study.Psoriasis (Auckland, N.Z.) · 2025Article
- HuR ablation destabilizesFrontiers in immunology · 2025Article
- Role of RNA-binding Proteins in Regulating Cell Adhesion and Progression of the Atherosclerotic Plaque and Plaque Erosion.Current atherosclerosis reports · 2024Review
- RNA-binding protein HuR reprograms immune T cells and promotes oral squamous cell carcinoma.Oral oncology reports · 2024Article
- RNA Metabolism Governs Immune Function and Response.Advances in experimental medicine and biology · 2024Review
- NK cell expansion requires HuR and mediates control of solid tumors and long-term virus infection.The Journal of experimental medicine · 2023Article
- Human IL-17A protein production is controlled through a PIP5K1α-dependent translational checkpoint.Science signaling · 2023Article
- RNA circuits and RNA-binding proteins in T cells.Trends in immunology · 2023Review
- Post-transcriptional checkpoints in autoimmunity.Nature reviews. Rheumatology · 2023Review
- Posttranscriptional Regulation of Gene Expression Participates in the Myelin Restoration in Mouse Models of Multiple Sclerosis: Antisense Modulation of HuR and HuD ELAV RNA Binding Protein.Molecular neurobiology · 2023Article
- RNA Metabolism in T Lymphocytes.Immune network · 2022Review
- The RNA-binding protein IMP2 drives a stromal-Th17 cell circuit in autoimmune neuroinflammation.JCI insight · 2022Article
- Targeting the RNA-Binding Protein HuR as Potential Thera-Peutic Approach for Neurological Disorders: Focus on Amyo-Trophic Lateral Sclerosis (ALS), Spinal Muscle Atrophy (SMA) and Multiple Sclerosis.International journal of molecular sciences · 2021Review
- Defining the RBPome of primary T helper cells to elucidate higher-order Roquin-mediated mRNA regulation.Nature communications · 2021Article
- Regulation of mRNA stability by RBPs and noncoding RNAs contributing to the pathogenicity of Th17 cells.RNA biology · 2021Review
- Conceptual Advances in Control of Inflammation by the RNA-Binding Protein Tristetraprolin.Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
IL-17 is a proinflammatory cytokine produced by activated Th17 cells and other immune cells. IL-17-producing Th17 cells are major contributors to chronic inflammatory and autoimmune diseases, such as multiple sclerosis, rheumatoid arthritis, and inflammatory bowel disease. Although the transcriptional regulation of Th17 cells is well understood, the posttranscriptional regulation of IL-17 gene expression remains unknown. The RNA-binding protein HuR positively regulates the stability of many target mRNAs via binding the AU-rich elements present in the 3' untranslated region of many inflammatory cytokines including IL-4, IL-13, and TNF-α. However, the regulation of IL-17 expression by HuR has not been established. CD4(+) Th17 cells from HuR knockout mice had decreased IL-17 steady-state mRNA and protein levels compared with wild-type Th17 cells, as well as decreases in frequency of IL-17(+) cells. Moreover, we demonstrated that HuR directly binds to the IL-17 mRNA 3' untranslated region by using RNA immunoprecipitation and biotin pulldown assays. In addition, the knockout of HuR decreased cellular proliferation of CD4(+) T cells. Mice with adoptively transferred HuR KO Th17 cells had delayed initiation and reduced disease severity in the onset of experimental autoimmune encephalomyelitis compared with wild-type Th17 cells. Our results reveal a HuR-induced posttranscriptional regulatory mechanism of Th17 differentiation that influences IL-17 expression. These findings may provide novel therapeutic targets for the treatment of Th17-mediated autoimmune neuroinflammation.
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