ArticleArthritis and rheumatism2013
Glucocorticoids suppress T cell function by up-regulating microRNA-98.
Article in Arthritis and rheumatism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 62 citations in OpenAlex.
- Revisiting the safety of short-term systemic corticosteroids.Biomedical journal · 2026Review
- Intervention of Fish (Foods (Basel, Switzerland) · 2026Article
- Glucocorticoids regulate the human non-coding genome.bioRxiv : the preprint server for biology · 2025Article
- The effect of baseline versus early glucocorticoid use on immune checkpoint inhibitor efficacy in patients with advanced NSCLC.Frontiers in oncology · 2025Article
- Ocular myasthenia gravis management.Frontiers in neurology · 2025Review
- [Clinical characteristics of cytokine release syndrome after haploidentical hematopoietic stem cell transplantation for thalassemia major].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2024Article
- Activated CD4Internal medicine (Tokyo, Japan) · 2024Article
- Immune surveillance and humoral immune responses in kidney transplantation - A look back at T follicular helper cells.Frontiers in immunology · 2023Review
- Non-serogroupableIDCases · 2023Article
- Massive macroglossia, a rare side effect of COVID-19: clinical, histologic, and genomic findings in COVID-19-positive versus COVID-19-negative patients.Oral and maxillofacial surgery · 2022Article
- Role of microRNAs and long non‑coding RNAs in glucocorticoid signaling (Review).International journal of molecular medicine · 2022Review
- Understanding the Effects of Age and T-Cell Differentiation on COVID-19 Severity: Implicating a Fas/FasL-mediated Feed-Forward Controller of T-Cell Differentiation.Frontiers in immunology · 2022Article
- Dysregulated Expression of Arterial MicroRNAs and Their Target Gene Networks in Temporal Arteries of Treatment-Naïve Patients with Giant Cell Arteritis.International journal of molecular sciences · 2021Article
- Methylprednisolone Induces Neuro-Protective Effects via the Inhibition of A1 Astrocyte Activation in Traumatic Spinal Cord Injury Mouse Models.Frontiers in neuroscience · 2021Article
- Brain-homing CD4Neurology(R) neuroimmunology & neuroinflammation · 2020Article
- Article
- Current and emerging therapeutics for neuromyelitis optica spectrum disorder: Relevance to the COVID-19 pandemic.Multiple sclerosis and related disorders · 2020Review
- Article
- MicroRNAs in Systemic Lupus Erythematosus: a Perspective on the Path from Biological Discoveries to Clinical Practice.Current rheumatology reports · 2020Review
- Myeloid-derived suppressor cells increase and inhibit donor-reactive T cell responses to graft intestinal epithelium in intestinal transplant patients.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2018Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveTo identify microRNAs (miRNAs) in human T cells that can explain known antiinflammatory properties of steroids.
methodsActivated human CD4+ T cells from healthy donors were exposed to 1 μM methylprednisolone (MP) in vitro and then subjected to miRNA and messenger RNA microarray analyses. Changes in expression profiles were recorded. Using quantitative polymerase chain reaction (qPCR), flow cytometry, and enzyme-linked immunosorbent assay (ELISA), we confirmed the suppression of predicted targets, and through miRNA transfection experiments, we could suggest mechanistic links.
resultsWe identified numerous steroid-responsive genes and miRNAs-many known and some novel-including multiple previously unknown proinflammatory genes suppressed by MP. Further studies using qPCR, flow cytometry, and ELISA demonstrated that methylprednisolone increased the expression of miRNA-98 (miR-98) and suppressed the levels of predicted targets, including interleukin-13 and 3 tumor necrosis factor receptors (TNFRs): Fas, FasL, and TNFR superfamily member 1B. Forced expression of miR-98 in T cells resulted in suppression of the same targets.
conclusionThe findings of this study demonstrate a link between miR-98 expression and the effects of MP and provide evidence suggesting that MP acts through miR-98 to inhibit specific proinflammatory targets. Identification of this antiinflammatory mechanism of glucocorticoids is important, since it may pave the way toward the elusive goal of dissociating adverse effects from therapeutic effects.
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Registered trials
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